3 years ago

Changes in remote myocardial tissue after acute myocardial infarction and its relation to cardiac remodeling: A CMR T1 mapping study

Niels van Royen, Peter M. van de Ven, Paul. F. A. Teunissen, Albert C. van Rossum, Lourens F. H. J. Robbers, Aernout M. Beek, P. Stefan Biesbroek, Robin Nijveldt, Mark B. M. Hofman, Raquel P. Amier

by P. Stefan Biesbroek, Raquel P. Amier, Paul. F. A. Teunissen, Mark B. M. Hofman, Lourens F. H. J. Robbers, Peter M. van de Ven, Aernout M. Beek, Albert C. van Rossum, Niels van Royen, Robin Nijveldt

Objectives

To characterize the temporal alterations in native T1 and extracellular volume (ECV) of remote myocardium after acute myocardial infarction (AMI), and to explore their relation to left ventricular (LV) remodeling.

Methods

Forty-two patients with AMI successfully treated with primary PCI underwent cardiovascular magnetic resonance after 4–6 days and 3 months. Cine imaging, late gadolinium enhancement, and T1-mapping (MOLLI) was performed at 1.5T. T1 values were measured in the myocardial tissue opposite of the infarct area. Myocardial ECV was calculated from native- and post-contrast T1 values in 35 patients, using a correction for synthetic hematocrit.

Results

Native T1 of remote myocardium significantly decreased between baseline and follow-up (1002 ± 39 to 985 ± 30ms, p<0.01). High remote native T1 at baseline was independently associated with a high C-reactive protein level (standardized Beta 0.32, p = 0.04) and the presence of microvascular injury (standardized Beta 0.34, p = 0.03). ECV of remote myocardium significantly decreased over time in patients with no LV dilatation (29 ± 3.8 to 27 ± 2.3%, p<0.01). In patients with LV dilatation, remote ECV remained similar over time, and was significantly higher at follow-up compared to patients without LV dilatation (30 ± 2.0 versus 27 ± 2.3%, p = 0.03).

Conclusions

In reperfused first-time AMI patients, native T1 of remote myocardium decreased from baseline to follow-up. ECV of remote myocardium decreased over time in patients with no LV dilatation, but remained elevated at follow-up in those who developed LV dilatation. Findings from this study may add to an increased understanding of the pathophysiological mechanisms of cardiac remodeling after AMI.

Publisher URL: http://journals.plos.org/plosone/article

DOI: 10.1371/journal.pone.0180115

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