Coronary Artery Disease and Acute Coronary Syndromes

Classification: Coronary artery disease is impaired coronary blood flow, usually from atherosclerosis. Acute coronary syndrome (ACS) includes unstable angina, NSTEMI, and STEMI and usually reflects acute plaque disruption with superimposed thrombus.

Key diagnostic discriminator: Stable angina is predictable demand-induced ischemia from fixed coronary narrowing and is not ACS. UA, NSTEMI, and STEMI are distinguished by myocardial necrosis, troponin release, and ECG pattern.

Clinical priority: Identify acute ischemia rapidly, determine whether infarction has occurred, and recognize the ECG pattern that signals severe ongoing injury and need for urgent reperfusion assessment.

Myocardial Oxygen Supply-Demand Balance

Coronary ischemia is best understood as a mismatch between myocardial oxygen supply and demand. Demand increases with heart rate, contractility, and ventricular wall stress. Supply depends on coronary perfusion pressure and duration, arterial oxygen content, and the ability of coronary vessels to augment flow. Fixed atherosclerotic stenosis primarily limits coronary flow reserve, whereas anemia, hypoxemia, hypotension, severe hypertension, or sustained tachyarrhythmia can create ischemia by altering supply or demand even without acute plaque rupture (Kusumoto, 2019; Norris, 2020; Rogers & Spinler, 2026).

Atherosclerosis and Stable Angina

Endothelial dysfunction, inflammation, lipid accumulation, and plaque formation progressively narrow coronary arteries. A fixed stenosis may provide adequate blood flow at rest but cannot increase flow sufficiently when heart rate, contractility, or blood pressure raise myocardial oxygen demand. This produces transient reversible ischemia without necrosis: stable angina (Norris, 2020; Rogers & Spinler, 2026).

How ACS Develops

ACS most commonly begins with plaque rupture, fissuring, or erosion. Platelet adhesion, activation, aggregation, and coagulation produce a fibrin-platelet thrombus that partially or completely reduces coronary flow. The severity and duration of ischemia determine whether injury remains reversible or progresses to cardiomyocyte necrosis (Norris, 2020; Rogers & Spinler, 2026).

Type 1 Versus Type 2 Myocardial Infarction

Type 1 MI is caused by an acute atherothrombotic coronary event, typically plaque disruption with superimposed thrombus. Type 2 MI reflects myocardial ischemia and infarction from an oxygen supply-demand imbalance without acute coronary atherothrombosis, such as severe anemia, sustained tachyarrhythmia, marked hypotension, or other physiologic stress. Both can produce troponin elevation, so the biomarker must be interpreted within the clinical mechanism rather than assumed to prove plaque rupture (Rogers & Spinler, 2026).

Stable Angina, UA, NSTEMI, and STEMI

Condition	Pathology	Typical symptom pattern	ECG concept	Troponin
Stable angina	Fixed flow-limiting stenosis; no acute thrombus required	Predictable with exertion/demand	Often normal at rest; ischemic change may appear with stress	Negative
Unstable angina	Acute ischemia, often partial/dynamic thrombus, without detectable necrosis	New, worsening, prolonged, or rest symptoms	May be normal, ST depression, or T-wave change; no persistent diagnostic ST elevation	Negative
NSTEMI	Acute MI with myocardial necrosis	Acute ischemic symptoms	No persistent diagnostic ST-elevation pattern; ST depression/T-wave changes may occur	Positive
STEMI	Acute MI with severe ongoing ischemia, usually acute thrombotic occlusion	Acute ischemic symptoms	Diagnostic ST-segment elevation pattern in appropriate leads	Positive

Ischemia Versus Infarction

Ischemia means oxygen supply is insufficient for myocardial demand but the tissue may remain viable. Infarction means ischemia has caused irreversible cardiomyocyte injury and necrosis. Membrane disruption releases cardiac troponin into the circulation. Troponin therefore helps distinguish NSTEMI from unstable angina in the appropriate ischemic clinical context (Norris, 2020; Rogers & Spinler, 2026).

STEMI and NSTEMI Terminology

STEMI and NSTEMI are clinically classified using the ECG, biomarker evidence of myocardial injury, and the clinical syndrome rather than by proving histologic depth of necrosis. Traditional descriptions of STEMI as “transmural” and NSTEMI as “subendocardial” can help illustrate typical injury patterns but should not be treated as defining criteria (Rao et al., 2025).

Complications of Myocardial Infarction

Electrical instability: VT, VF, bradyarrhythmias, and conduction block (Norris, 2020; Rogers & Spinler, 2026).
Pump failure: acute HF, pulmonary edema, or cardiogenic shock (Norris, 2020; Rogers & Spinler, 2026).
Mechanical injury: papillary muscle dysfunction/rupture, septal rupture, or free-wall rupture (Norris, 2020; Rogers & Spinler, 2026).
Long-term remodeling: dilation, fibrosis, hypertrophy, and chronic HF (Norris, 2020; Rogers & Spinler, 2026).

Diagnostic Approach

Integrate symptom onset and pattern with serial ECGs and serial high-sensitivity cardiac troponin measurements (Norris, 2020; Rogers & Spinler, 2026).
A normal initial ECG does not exclude ischemia (Norris, 2020; Rogers & Spinler, 2026).
Use echocardiography or coronary imaging when clinically indicated to assess ventricular function, wall-motion abnormalities, anatomy, or complications (Norris, 2020; Rogers & Spinler, 2026).

Clinical Manifestations

Myocardial ischemia may produce substernal pressure, heaviness, squeezing, or discomfort with radiation to the arm, shoulder, neck, jaw, or back. Dyspnea, diaphoresis, nausea, fatigue, and weakness may accompany or replace classic chest discomfort. Stable angina is predictable with demand; ACS symptoms are more likely to be new, prolonged, worsening, or present at rest (Norris, 2020; Rogers & Spinler, 2026).

Findings That Alter the Differential

A normal initial ECG does not exclude ischemia. Serial ECGs and serial cardiac troponin measurements are often necessary because both electrical and biomarker abnormalities evolve over time. Troponin indicates myocardial injury and must be interpreted with the ischemic presentation and ECG rather than treated as specific for coronary thrombosis by itself (Rao et al., 2025).

Differential Diagnosis

Life-threatening alternatives to acute coronary ischemia include pulmonary embolism, acute aortic syndromes, pericarditis, myocarditis, and pneumothorax. Pneumonia, gastrointestinal disease, and musculoskeletal pain may also mimic ischemic symptoms. Symptom quality alone cannot safely exclude ACS or these competing diagnoses (Rao et al., 2025).

Treatment Principles

Stable coronary disease management aims to reduce ischemic symptoms, improve the myocardial oxygen supply-demand relationship, and reduce future cardiovascular events. ACS management additionally targets acute platelet/coagulation-driven thrombosis and restoration of coronary perfusion when indicated. The specific antithrombotic and reperfusion strategy depends on STEMI versus NSTE-ACS, timing, bleeding risk, and coronary anatomy (Rao et al., 2025; Rogers & Spinler, 2026).

Red Flags

New or persistent ischemic chest pressure at rest (Norris, 2020; Rogers & Spinler, 2026).
Diagnostic ST-segment elevation or dynamic ischemic ECG changes (Norris, 2020; Rogers & Spinler, 2026).
A rising/falling troponin pattern with clinical evidence of acute myocardial ischemia (Norris, 2020; Rogers & Spinler, 2026).
Hemodynamic instability, ventricular arrhythmia, acute pulmonary edema, or cardiogenic shock (Rao et al., 2025).

High-Yield Distinctions

Stable angina is chronic coronary disease, not ACS.
Unstable angina = ischemia without detectable myocardial necrosis.
NSTEMI = infarction with positive troponin but no persistent diagnostic ST-elevation pattern.
STEMI = infarction with a diagnostic ST-elevation pattern in the appropriate clinical context.
Plaque disruption and acute thrombus formation are central to most type 1 ACS.

Related YourDNP Resources

Content last reviewed:

September 30, 2026

References

Kusumoto, F. M. (2019). Cardiovascular disorders: Heart disease. In G. D. Hammer & S. J. McPhee (Eds.), Pathophysiology of disease: An introduction to clinical medicine (8th ed., pp. 289–328). McGraw-Hill Education.

Norris, T. L. (2020). Porth’s essentials of pathophysiology (5th ed.). Wolters Kluwer.

Rao, S. V., O’Donoghue, M. L., Ruel, M., Rab, T., Tamis-Holland, J. E., Alexander, J. H., Baber, U., Baker, H., Cohen, M. G., Cruz-Ruiz, M., Davis, L. L., de Lemos, J. A., DeWald, T. A., Elgendy, I. Y., Feldman, D. N., Goyal, A., Isiadinso, I., Menon, V., Morrow, D. A., … Williams, M. S. (2025). 2025 ACC/AHA/ACEP/NAEMSP/SCAI guideline for the management of patients with acute coronary syndromes. Circulation, 151(13), e771–e862. https://doi.org/10.1161/CIR.0000000000001309

Rogers, K. C., & Spinler, S. A. (2026). Acute coronary syndromes. In M. A. Chisholm-Burns, P. M. Malone, J. M. Kolesar, K. C. Lee, P. B. Bookstaver, & K. R. Matthias (Eds.), Pharmacotherapy principles & practice (7th ed.). McGraw Hill.