What is the difference between angina (angina pectoris) and myocardial infarction (heart attack)?

Difference Between Angina and Myocardial Infarction

The fundamental difference is that myocardial infarction involves actual death of heart muscle cells (myocardial necrosis) with elevated cardiac troponin levels, while angina represents reversible myocardial ischemia without cell death and normal troponin levels. 1, 2

Key Distinguishing Features

Myocardial Necrosis

• Myocardial infarction is defined by elevated cardiac biomarkers (troponin above the 99th percentile upper reference limit) indicating definite myocardial injury, combined with symptoms of ischemia, new ECG changes, or imaging evidence of new wall motion abnormalities 1, 3
• Angina (particularly unstable angina) represents myocardial ischemia of insufficient severity and duration to cause myocardial necrosis, with troponin levels remaining below the 99th percentile on at least 2 samples collected ≥6 hours apart 1, 2, 3

Clinical Presentation Differences

• Angina typically presents as chest discomfort that is reversible, either spontaneously or with nitroglycerin, lasting minutes to up to 20 minutes 1
• Myocardial infarction presents with more prolonged chest pain (typically >20 minutes) that does not fully resolve with nitroglycerin and represents ongoing myocardial damage 1
• Stable angina occurs predictably with exertion and resolves with rest, while unstable angina occurs at rest or with minimal exertion 1

Diagnostic Algorithm

Step 1: Obtain serial troponin measurements

• A single negative troponin is insufficient; obtain at least 2 samples ≥6 hours apart 2
• High-sensitivity troponin assays have increased MI detection by 20% relative increase, reclassifying many cases previously diagnosed as unstable angina to NSTEMI 2, 3

Step 2: Assess ECG findings

• Myocardial infarction (NSTEMI) shows persistent ST-segment depression, T-wave inversion, or transient ST-elevation with elevated troponin 1, 2
• Unstable angina may show similar ECG changes but troponin remains normal; approximately 5% have completely normal ECG even during symptoms 2
• ST-segment elevation MI (STEMI) shows persistent ST-elevation or new left bundle branch block requiring immediate reperfusion 1

Step 3: Determine underlying mechanism

• Type 1 MI results from atherosclerotic plaque rupture with intraluminal thrombus formation 1
• Type 2 MI occurs from oxygen supply-demand mismatch (hypotension, anemia, hypoxemia, tachyarrhythmias) without plaque rupture 1, 3
• Angina can result from progressive atherosclerosis, coronary vasospasm, microvascular dysfunction, or secondary causes increasing oxygen demand 1

Prognostic Implications

Mortality Risk

• NSTEMI carries significantly higher mortality than unstable angina: 30-day mortality is 3.7-7.4% for NSTEMI versus 0.5-0.7% for unstable angina 4
• One-year mortality for NSTEMI is 10.4-22.9% compared to 3.3-5.1% for unstable angina, with unstable angina mortality similar to non-cardiac chest pain 4
• Women with STEMI have higher mortality even after adjusting for baseline characteristics and revascularization strategies 1

Future Cardiac Events

• Despite lower mortality, unstable angina carries similar risk of future non-fatal MI as NSTEMI (11.2% vs 7.9% in one study), both substantially higher than non-cardiac chest pain 4
• Patients with stable angina and coronary artery disease have increased risk for heart failure, cardiovascular hospitalization, and need for coronary revascularization 5

Management Differences

Antiplatelet Therapy Intensity

• NSTEMI patients derive greater benefit from more potent P2Y12 inhibitors (ticagrelor, prasugrel) compared to unstable angina patients 3
• Unstable angina patients have less benefit from intensified antiplatelet therapy given the absence of myocardial necrosis 2

Invasive Strategy Timing

• NSTEMI patients benefit more from early invasive strategy (coronary angiography within 72 hours) 3
• Unstable angina patients have less benefit from early invasive approach but still require risk stratification using GRACE score 3
• High-risk features mandating urgent evaluation include accelerating symptoms, prolonged rest pain, pulmonary edema, new mitral regurgitation murmur, or significant ECG changes 2

Common Pitfalls

Diagnostic Errors

• Failing to obtain serial troponin measurements is the most common error; the distinction between unstable angina and NSTEMI may not be apparent at initial presentation 2, 3
• Atypical presentations are common in elderly patients (>75 years), diabetics, women, and those with chronic kidney disease, who may present with epigastric pain, dyspnea, or weakness rather than classic chest pain 1, 2
• Younger women (<50 years) are more likely to have non-obstructive causes including coronary microvascular dysfunction, vasospasm, or spontaneous coronary artery dissection rather than classic plaque rupture 1

Pathophysiologic Considerations

• The absence of obstructive coronary disease on angiography does not exclude significant ischemia; myocardial infarction with non-obstructive coronary arteries (MINOCA) accounts for a substantial proportion of cases, particularly in women 1
• Coronary microvascular dysfunction, vasospasm, and spontaneous coronary artery dissection can cause both angina and MI without visible epicardial stenosis 1, 6
• Secondary causes (fever, tachycardia, thyrotoxicosis, hypotension, anemia, hypoxemia) can precipitate angina in patients with underlying coronary disease or cause type 2 MI 1