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Radiology · Chest Radiology

Diagnostic imaging of myocardial infarction

Infarctus myocardii

Diagnostic imaging of myocardial infarction focuses on the precise visualization of myocardial ischemia, edema, and necrosis. The leading method for detailed assessment of injury, including the no-reflow phenomenon, is late gadolinium enhancement magnetic resonance imaging (CMR LGE).

High precisionMRI detects areas of irreversible myocardial injury starting from 1 ml in volume.
Scan timingOptimally performed 10–25 minutes after the administration of gadolinium chelates.
Necrosis localizationTypically located subendocardially within the basin of the affected artery.
Aborted myocardial infarctionNo necrosis is present, no contrast uptake, and the myocardial salvage index is 100%.
4 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Comparison of imaging modalities

Several imaging modalities are used to diagnose acute myocardial infarction and its consequences, each serving specific purposes:

  • Traditional chest X-ray (performed at the bedside) allows for the detection of moderate cardiomegaly and the assessment of the presence or absence of pulmonary edema.
  • Contrast left ventriculography during cardiac catheterization visualizes extensive areas of reduced contractility at end-systole (e.g., of the apicoinferior or anterior wall).
  • Echocardiography (EchoCG) reliably confirms data on regional wall motion abnormalities in real time.
  • Magnetic resonance imaging (MRI) is considered the most accurate method. Cine MRI (Cine CMR) assesses functional consequences in detail, demonstrating areas of akinesia, while contrast-enhanced sequences allow for the visualization of the necrotic zone itself.

Late gadolinium enhancement cardiac magnetic resonance (LGE CMR)

A true breakthrough in myocardial infarction imaging was the introduction of the inversion-recovery sequence for $T_1$-weighted images. The delayed enhancement method is based on the difference in longitudinal relaxation times between normal and infarcted tissue.

Patients are administered intravenous gadolinium chelates, which distribute within the extracellular space. The volume of distribution of the agent is maximal precisely in the necrotic portion of the myocardium. This leads to a marked shortening of the $T_1$ relaxation time. Scanning is performed 10–25 minutes post-injection. On the scans, the infarction zone appears as a bright area of intense subendocardial contrast accumulation that strictly corresponds to the blood supply basin of the affected coronary artery. The method can detect injury foci weighing less than 1 gram, which is important, for example, when searching for a cardiac source of embolism in ischemic stroke.

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Parametric imaging: T1 and T2 mapping

For pixel-by-pixel analysis of tissue relaxation behavior, parametric imaging methods are used—$T_1$ and $T_2$ mapping (mapping), often with color coding.

$T_1$ and $T_2$ values increase in the myocardium at risk (in the edema zone), which allows for the precise calculation of the area of the area at risk. Post-contrast $T_1$ mapping demonstrates the lowest values directly within the area of myocardial necrosis.

Based on these data, the myocardial salvage index (Myocardial Salvage Index) is calculated. It is computed by comparing the area of irreversible necrosis with the area of myocardial edema. Assessing the volume of salvaged tissue has the highest prognostic value for the patient.

Reperfusion injury and the no-reflow phenomenon

Half of the patients with successfully reperfused ST-elevation myocardial infarction (STEMI) develop reperfusion injury.

  1. Microvascular obstruction (the no-reflow phenomenon) is the occlusion of capillaries in the center of the infarction zone. On the ECG, this manifests as persistent ST-elevation, and on contrast-enhanced MRI scans, the obstruction appears as a central "dark zone" that does not accumulate the contrast agent within the bright infarction area.
  2. Hemorrhagic infarction is the extravasation of red blood cells due to severe microcirculatory bed damage. Deoxyhemoglobin possesses paramagnetic properties; therefore, on $T_2$-weighted images, intramyocardial hemorrhage is also visualized as a central dark zone.

Both of these phenomena reflect severe tissue damage and serve as predictors of an adverse prognosis.

Visualization of complications

Myocardial infarction may be accompanied by secondary reactions that are clearly distinguishable on MRI. For example, in acute transmural injury of the left ventricular wall, the inflammatory process can extend to the outer layers of the heart.

On $T_2$-weighted images, in addition to the hyperintense signal from myocardial edema itself, a bright signal from fluid accumulation along the wall may be observed. On delayed scans (LGE CMR), the pericardium itself begins to diffusely accumulate contrast. This is a direct sign of reactive inflammation—secondary pericarditis associated with a prior myocardial infarction. For the precise localization of all findings, radiologists traditionally use the standardized 17-segment model of the heart.

Briefly: answers to topical questions

What complications of myocardial infarction, besides pericarditis, can be visualized using MRI?

MRI allows visualization of myocardial reperfusion injury.

These include:

  • Microvascular obstruction (no-reflow) is the occlusion of the microvasculature in the center of the infarct zone; on contrast-enhanced MRI, it is defined as the absence of contrast enhancement ("dark zone") in the center of the infarction area.
  • Hemorrhagic infarction (haemorrhagic infarction) is the extravasation of erythrocytes due to severe capillary damage; on T2-weighted images, intramyocardial hemorrhage appears as a central "dark zone".

Which echocardiographic signs indicate acute myocardial infarction?

The main echocardiographic sign of acute myocardial infarction is the presence of left ventricular regional wall motion abnormality zones.

The following types of such abnormalities are distinguished:

  • Hypokinesia — decreased amplitude or force of myocardial contraction.
  • Akinesia — complete absence of contraction in the affected area.
  • Dyskinesia — paradoxical movement (bulging) of the wall during systole.
How to memorize

Bright necrosis, dark obstruction: with late gadolinium enhancement, dead tissue "glows" (takes up contrast), while the zone of microvascular obstruction remains dark because the agent cannot penetrate there through occluded capillaries.

Class and exam questions

Why is the MRI scan performed 10–25 minutes after gadolinium administration?

This time is necessary for the contrast agent to be maximally washed out from healthy areas and accumulate in the expanded extracellular space of the necrotic tissue, creating optimal tissue contrast.

What does the concept of "aborted myocardial infarction" mean on MRI?

This is a clinical situation where necrosis has not developed due to rapid restoration of blood flow. MRI visualizes edema (zone at risk), but there are no areas of contrast enhancement, and the myocardial salvage index is 100%.

How does microvascular obstruction look on tomograms?

It is visualized as a dark area (absence of contrast agent enhancement) right in the center of the bright, enhanced infarct region.

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What else to study on this topic

  • Pathophysiology of T1 and T2 relaxation time changes in edema and necrosis
  • Application of the 17-segment myocardial model in diagnostic imaging
  • Association of microfocal myocardial injuries with ischemic cerebrovascular accidents
  • Algorithms for calculating the area at risk and Myocardial Salvage Index
  • Hemodynamic parameters and contractility assessment in Cine CMR mode

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