# Native T1-mapping using cardiovascular magnetic resonance detects myocardium at risk during the first week following myocardial infarction in a swine model and in patients - comparison to contrast-enhanced cine steady-state free precession

**Authors:** Theodor Lav, David Nordlund, Christos Xanthis, Jonathan Berg, Sebastian Bidhult, Anthony H. Aletras, Robert Jablonowski

PMC · DOI: 10.1186/s12872-026-05507-3 · BMC Cardiovascular Disorders · 2026-01-22

## TL;DR

This study shows that native T1-mapping can detect heart muscle at risk after a heart attack without using contrast agents, but it overestimates the size of the damaged area.

## Contribution

Native T1-mapping is shown to agree with CE-SSFP for myocardium at risk but overestimates infarct size compared to LGE in both pigs and patients.

## Key findings

- Native T1-mapping MOLLI agreed with CE-SSFP in pigs and patients for myocardium at risk.
- MOLLI overestimated infarct size compared to LGE in both pigs and patients.
- SASHA T1-mapping also agreed with CE-SSFP in serially imaged pigs.

## Abstract

Myocardium at risk (MaR) can be evaluated by cardiovascular magnetic resonance (CMR) imaging using contrast-enhanced steady state free precession (CE-SSFP) in patients after ST-elevation myocardial infarction (STEMI). However, CE-SSFP utilizes gadolinium contrast, which is contraindicated in patients with severe renal insufficiency. Native T1-mapping is a non-contrast CMR method which has been shown feasible in assessing MaR, enabling patients with gadolinium contrast contraindications to be examined. However, native T1-mapping data have been presented in the sub-acute phase suggesting to also depict infarct size (IS), as assessed by late gadolinium enhancement (LGE). Therefore, it is unclear whether native T1-mapping depicts MaR or IS during the first week after reperfusion. We hypothesized that native T1-mapping agrees with MaR as assessed by CE-SSFP and overestimates IS as assessed by LGE in an experimental pig model and in patients during the first week after STEMI.

A retrospective analysis was performed using CMR images from an infarct/reperfusion experimental pig model. CMR imaging was performed at 2 h, 24 h and 7 days after reperfusion in a serially imaged group (n = 7) and at 4 days in a single-timepoint imaged group (n = 4). Also, STEMI patients with a single vessel LAD occlusion (n = 11) were CMR imaged between 3 to 7 days after reperfusion. Native T1-mapping MOLLI, CE-SSFP and LGE were acquired for each scan in both animals and patients. In animals, images with an additional T1-mapping sequence, SASHA, were acquired. Enhanced areas on T1-maps, CE-SSFP and LGE images were quantified and compared.

In pigs, native T1-mapping MOLLI agreed with CE-SSFP in the single-timepoint- and serially imaged groups (bias: 0.3 ± 6.6% (mean ± 2SD), and 0.9 ± 18%), respectively. Native T1-mapping SASHA also agreed with CE-SSFP in the serially imaged group (bias: -0.1 ± 18%). However, MOLLI overestimated IS by LGE in pigs in the serially- and single-timepoint imaged groups (bias: 21 ± 26%, and 18 ± 17%), respectively. Similar results were seen in patients (MOLLI vs. CE-SSFP: 0.8 ± 7.5%, and MOLLI vs. LGE: 31 ± 22%).

Our findings suggest that native T1-mapping agrees with CE-SSFP during the first week after myocardial infarction when evaluating MaR. Also, native T1-mapping overestimates the LGE hyperintense area, indicating that native T1-mapping does not primarily depict infarct size.

The online version contains supplementary material available at 10.1186/s12872-026-05507-3.

## Linked entities

- **Diseases:** myocardial infarction (MONDO:0005068), ST-elevation myocardial infarction (MONDO:0041656)
- **Species:** Sus scrofa (taxon 9823), Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** RBBP4 (RB binding protein 4, chromatin remodeling factor) [NCBI Gene 5928] {aka NURF55, RBAP48, lin-53}
- **Diseases:** edema (MESH:D004487), ischemia (MESH:D007511), Death (MESH:D003643), microvascular obstruction (MESH:D017566), reperfusion injury (MESH:D015427), myocardial infarction (MESH:D009203), ischemic pain (MESH:D010146), LAD occlusion (MESH:D001157), necrotic (MESH:D009336), overdose (MESH:D062787), LAD occlusion (MESH:C535887), arrythmia (MESH:D001145), MaR (MESH:D017682), circulatory collapse (MESH:D012769), ischemic (MESH:D002545), ST-elevation myocardial infarction (MESH:D000072657), LAD infarctions (MESH:D002544), IS (MESH:D007238), kidney insufficiency (MESH:D051437), LGE (MESH:C564835), nephrogenic systemic fibrosis (MESH:D054989), SASHA (MESH:D012640), MOLLI (MESH:D007446), coronary occlusion (MESH:D054059), hemorrhage (MESH:D006470)
- **Chemicals:** Gd-DOTA (MESH:C050823), pentobarbital (MESH:D010424), Gadolinium (MESH:D005682), Isoflurane (MESH:D007530), water (MESH:D014867), CE (MESH:D002563), Fentanyl (MESH:D005283), CMR (-)
- **Species:** Sus scrofa (pig, species) [taxon 9823], Homo sapiens (human, species) [taxon 9606], Canis lupus familiaris (dog, subspecies) [taxon 9615]

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12849553/full.md

## References

3 references — full list in the complete paper: https://tomesphere.com/paper/PMC12849553/full.md

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Source: https://tomesphere.com/paper/PMC12849553