Ischemic cascade and myocardial injury
During coronary artery occlusion, events develop in a strict sequence known as the ischemic cascade:
- Metabolic abnormalities (drop in ATP levels).
- Diastolic dysfunction (impaired relaxation).
- Systolic dysfunction (impaired contraction).
- Regional wall motion abnormalities.
- ECG changes.
- Onset of anginal pain.
The fate of cardiomyocytes depends on the duration of ischemia. Up to 20–30 minutes, changes are completely reversible. If ischemia lasts longer, irreversible injury begins—myocardial infarction. Necrosis always starts in the inner layers (subendocardium) and gradually (over 3–6 hours) spreads across the entire wall thickness toward the epicardium.
Infarction evolution and remodeling
Infarction triggers cardiac remodeling, which alters ventricular shape and size.
- Early phase: edema, hemorrhage, inflammation. The wall weakens, and the infarct zone expands. During this period, the risk of wall rupture or acute aneurysm formation is high.
- Healing: dead tissue is gradually replaced by a dense fibrous scar rich in collagen. The wall thins.
To compensate for the loss of contractile tissue and maintain stroke volume, the ventricle dilates (dilatation). Over time, this can lead to ischemic cardiomyopathy and severe heart failure.
Viable myocardium states
Not every dysfunction implies cell death. Under conditions of ischemia, the myocardium can enter specific states:
- Stunned myocardium (stunned myocardium): occurs after brief ischemia (<15 minutes). Cells are alive, there is no infarction, but their function recovers with a delay even after blood flow is restored.
- Hibernating myocardium (hibernating myocardium): adaptation to prolonged but mild ischemia. Cells sharply reduce energy consumption and stop contracting to survive. If blood supply is restored, function will eventually return to normal.
CAD imaging: angiography and tomography
The primary invasive method remains traditional coronary angiography (CAG). A significant lesion is considered a stenosis of $\ge$50% in the left main coronary artery or $\ge$50% in any major artery (or $\ge$70% in any major artery).
Limitations of CAG:
- Does not visualize plaques that do not narrow the lumen, even though their rupture most frequently causes infarction.
- Provides no information on plaque composition.
- A normal angiogram does not rule out CAD (e.g., in microvascular dysfunction affecting small vessels).
Therefore, non-invasive methods are increasingly used: CT coronary angiography (CCT) with coronary calcium scoring and cardiac MRI (CMR). Treatment (stenting) should be performed only for stenosis that genuinely causes ischemia, avoiding unjustified interventions (the "oculo-stenotic reflex").
Briefly: answers to topical questions
Which MRI features indicate the presence of viable myocardium?
Myocardial viability on cardiac MRI is assessed by the following parameters:
- Contractile reserve — dysfunctional myocardium contracts or improves contractility upon stimulation, such as with dobutamine.
- Myocardial wall thickness.
- Integrity of myocyte cell membranes.
- Myocardial metabolism.
- Extracellular volume fraction (ECV).
In reversibly injured myocardium, ECV is elevated, while necrosis shows the highest ECV values. Non-viable myocardium shows no functional improvement or demonstrates worsening wall motion upon stimulation.
How is the coronary artery calcium score calculated on CT?
To quantify coronary calcium on CT, the Agatston score (Agatston score) is most commonly used. Less frequently, calcium volume or mass measurements are used. The assessment is performed on non-contrast cardiac computed tomography, after which the obtained values are compared with age- and sex-stratified reference databases.
What non-invasive imaging methods are used in CAD?
A wide range of non-invasive imaging modalities is used for diagnosing coronary artery disease. These include:
- Computed tomography (Cardiac Computed Tomography) — CT coronary angiography and stress CT perfusion.
- Magnetic resonance imaging (Cardiovascular Magnetic Resonance) — stress perfusion and functional CMR.
- Echocardiography — stress echocardiography with physical or pharmacological load.
- Radionuclide diagnostics — myocardial scintigraphy, perfusion SPECT (SPECT), and PET (PET) with functional tests.
- Hybrid imaging — SPECT/CT (SPECT/CT) and PET/CT (PET/CT).
What types of atherosclerotic plaques exist according to CT coronary angiography?
According to CT coronary angiography and coronary calcium scoring, the following are distinguished:
- Calcified plaques — detected on non-contrast CT with coronary calcium scoring.
- Non-calcified plaques — may be missed on isolated coronary calcium scoring and are detected by CT angiography.
Depending on the degree of stenosis, plaques are described as stenotic, minimally stenotic, and non-stenotic. Acute myocardial infarction is in most cases caused by the rupture of non-stenotic or minimally stenotic plaques.
Class and exam questions
What is the "wavefront" phenomenon in myocardial infarction?
This is the pattern of necrosis propagation. Cell death always starts in the subendocardium (inner layer) and progressively moves outward toward the epicardium.
How does hibernating myocardium differ from a scar?
Hibernating myocardium is alive but "dormant" due to chronic oxygen shortage; its function will recover after revascularization. A scar is dead tissue (collagen) that will no longer contract.
Why is chest pain a poor early marker of ischemia?
According to the ischemic cascade, anginal pain appears at the very end, after metabolic abnormalities have already occurred, wall motion has ceased, and ECG changes have developed.
What else to study on this topic
- Pathophysiology of microvascular dysfunction
- Assessment of fractional flow reserve (FFR)
- Morphological composition of a fresh thrombus under an electron microscope
- CT Coronary Angiography and Calcium Scoring Protocols
- Mechanisms of Myocardial Preconditioning
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