Fast T2 gradient-spin-echo (T2-GraSE) mapping for myocardial edema quantification: first in vivo validation in a porcine model of ischemia/reperfusion

Fernández‐Jiménez, Rodrigo; Sánchez‐González, Javier; Agüero, J.; Trigo, María Del; Galán‐Arriola, Carlos; Fuster, Valentín; Ibáñez, Borja

doi:10.1186/s12968-015-0199-9

Cited by 70 publications

(63 citation statements)

References 38 publications

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“…At all time points, the imaging protocol included a standard segmented cine steady-state free-precession sequence to provide highquality anatomic references; a T2-weighted short-tau triple inversion-recovery (T2W-STIR) sequence to assess the extent of edema and intramyocardial hemorrhage (IMH); and a T2-gradient-spin-echo mapping sequence to provide precise myocardial T2 relaxation time properties. 16 On day 7 and day 40 CMR, LGE imaging was performed to assess infarct size and microvascular obstruction (MVO), using a T1-weighted inversion recovery turbo field echo sequence acquired 10 to 15 minutes after intravenous administration of 0.20 mmol gadobutrol contrast agent per kg body weight.…”

Section: Cmr Protocolmentioning

confidence: 99%

“…CMR examinations were conducted with a Philips 3-Tesla Achieva Tx whole body scanner (Philips Healthcare) equipped with a 32-element phased-array cardiac coil. The imaging protocol included an steady-state free-precession sequence to provide high-quality anatomic references, and assessment of LV mass and wall thickness; a T2W-STIR sequence to assess the extent of edema and IMH; a T2-gradient-spinecho mapping sequence 10,16 ; and a T1-weighted inversion recovery turbo field echo sequence to assess IS and MVO. CMR images were similarly analyzed using dedicated software (MR Extended Work Space 2.6, Philips Healthcare; and QMassMR 7.6, Medis) by 2 observers experienced in CMR analysis and blinded to group allocation.…”

Section: Cmr Protocol and Analysismentioning

confidence: 99%

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Response by Fernández-Jiménez et al to Letters Regarding Article, “Dynamic Edematous Response of the Human Heart to Myocardial Infarction: Implications for Assessing Myocardial Area at Risk and Salvage”

et al. 2018

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BACKGROUND: Clinical protocols aimed to characterize the post-myocardial infarction (MI) heart by cardiac magnetic resonance (CMR) need to be standardized to take account of dynamic biological phenomena evolving early after the index ischemic event. Here, we evaluated the time course of edema reaction in patients with ST-segment-elevation MI by CMR and assessed its implications for myocardium-at-risk (MaR) quantification both in patients and in a large-animal model. METHODS: A total of 16 patients with anterior ST-segment-elevation MI successfully treated by primary angioplasty and 16 matched controls were prospectively recruited. In total, 94 clinical CMR examinations were performed: patients with ST-segment-elevation MI were serially scanned (within the first 3 hours after reperfusion and at 1, 4, 7, and 40 days), and controls were scanned only once. T2 relaxation time in the myocardium (T2 mapping) and the extent of edema on T2-weighted short-tau triple inversion-recovery (ie, CMR-MaR) were evaluated at all time points. In the experimental study, 20 pigs underwent 40-minute ischemia/reperfusion followed by serial CMR examinations at 120 minutes and 1, 4, and 7 days after reperfusion. Reference MaR was assessed by contrast-multidetector computed tomography during the index coronary occlusion. Generalized linear mixed models were used to take account of repeated measurements. RESULTS: In humans, T2 relaxation time in the ischemic myocardium declines significantly from early after reperfusion to 24 hours, and then increases up to day 4, reaching a plateau from which it decreases from day 7. Consequently, edema extent measured by T2-weighted short-tau triple inversion-recovery (CMR-MaR) varied with the timing of the CMR examination. These findings were confirmed in the experimental model by showing that only CMR-MaR values for day 4 and day 7 postreperfusion, coinciding with the deferred edema wave, were similar to values measured by reference contrast-multidetector computed tomography. CONCLUSIONS: Post-MI edema in patients follows a bimodal pattern that affects CMR estimates of MaR. Dynamic changes in post-ST-segment-elevation MI edema highlight the need for standardization of CMR timing to retrospectively delineate MaR and quantify myocardial salvage. According to the present clinical and experimental data, a time window between days 4 and 7 post-MI seems a good compromise solution for standardization. Further studies are needed to study the effect of other factors on these variables.

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Section: Cmr Protocolmentioning

confidence: 99%

Section: Cmr Protocol and Analysismentioning

confidence: 99%

Response by Fernández-Jiménez et al to Letters Regarding Article, “Dynamic Edematous Response of the Human Heart to Myocardial Infarction: Implications for Assessing Myocardial Area at Risk and Salvage”

et al. 2018

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“…Swine are commonly used for large animal models in cardiovascular research due to their similarities in heart size and coronary anatomy to the human . Many ischemia reperfusion porcine models, including Yorkshire and Göttingen pigs, have been well characterized with cardiac magnetic resonance (CMR) . Each animal model has its own specific advantages.…”

Section: Introductionmentioning

confidence: 99%

Multiparametric CMR imaging of infarct remodeling in a percutaneous reperfused Yucatan mini‐pig model

et al. 2017

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Purpose To further understanding of the temporal evolution and pathophysiology of adverse ventricular remodeling over the first 60 days following a myocardial infarction (MI) in both the infarcted and remote myocardium, we performed multi-parametric cardiac magnetic resonance imaging (CMR) in a closed-chest chronic Yucatan mini-pig model of reperfused MI. Methods Ten animals underwent 90 minute left anterior descending artery occlusion and reperfusion. Three animals served as controls. Multiparametric CMR (1.5T) was performed at baseline, day-2, day-30 and in four animals at day-60 post-MI. Left ventricular volumes and infarct size were measured. T1 and T2 Mapping sequences were performed to measure values in the infarct and remote regions. Remote region collagen fractions were compared between infarcted animals and controls. Results Procedure success was 80%. The model created large infarcts (28 ± 5% of left ventricular mass on day-2), which led to significant adverse myocardial remodeling that stabilized beyond 30 days. Native T1 values did not reliably differentiate remote and infarct regions acutely. There was no evidence of remote fibrosis as indicated by partition coefficient and collagen fraction analyses. The infarct T2 values remained elevated up to 60 days post-MI. Conclusion Multiparametric CMR in this model showed significant adverse ventricular remodeling 30 days post-MI similar to that seen in humans. In addition, this study demonstrated that remote fibrosis is absent and that infarct T2 signal remains chronically elevated in this model. These findings need to be considered when designing pre-clinical trials using CMR endpoints.

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“…Previous reports have described a correlation between T2 and total water content in IR models . After extensive myocardial infarction, cell membranes lose their integrity, and intra‐ and extracellular water compartments mix.…”

Section: Discussionmentioning

confidence: 92%

Measuring Water Distribution in the Heart: Preventing Edema Reduces Ischemia–Reperfusion Injury

Andrés‐Villarreal¹,

Barba²,

Poncelas³

et al. 2016

JAHA

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BackgroundEdema is present in many heart diseases, and differentiation between intracellular (ICW) and extracellular (ECW) myocardial water compartments would be clinically relevant. In this work we developed a magnetic resonance imaging–based method to differentiate ICW and ECW and applied it to analyze ischemia–reperfusion–induced edema.Methods and ResultsIsolated rat hearts were perfused with gadolinium chelates as a marker of extracellular space. Total water content was measured by desiccation. Gadolinium quantification provided ECW, and ICW was calculated by subtraction of ECW from total water content. In separate experiments, T1, T2, diffusion‐weighted imaging and proton‐density parameters were measured in isolated saline‐perfused hearts. In in‐situ rat hearts, ECW and ICW were 79±10 mL and 257±8 mL of water per 100 g of dry tissue, respectively. After perfusion for 40 minutes, ECW increased by 92.4±3% without modifying ICW (−1±3%). Hyposmotic buffer (248 mOsm/L) increased ICW by 16.7±2%, while hyperosmotic perfusion (409 mOsm/L) reduced ICW by 26.5±3%. Preclinical imaging showed good correlation between T2 and diffusion‐weighted imaging with ECW, and proton‐density correlated with total water content. Ischemia–reperfusion resulted in marked myocardial edema at the expense of ECW, because of cellular membrane rupture. When cell death was prevented by blebbistatin, water content and distribution were similar to normoxic perfused hearts. Furthermore, attenuation of intracellular edema with hyperosmotic buffer reduced cell death.ConclusionsWe devised a method to determine edema and tissue water distribution. This method allowed us to demonstrate a role of edema in reperfusion‐induced cell death and could serve as a basis for the study of myocardial water distribution using magnetic resonance imaging.

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Fast T2 gradient-spin-echo (T2-GraSE) mapping for myocardial edema quantification: first in vivo validation in a porcine model of ischemia/reperfusion

Cited by 70 publications

References 38 publications

Response by Fernández-Jiménez et al to Letters Regarding Article, “Dynamic Edematous Response of the Human Heart to Myocardial Infarction: Implications for Assessing Myocardial Area at Risk and Salvage”

Response by Fernández-Jiménez et al to Letters Regarding Article, “Dynamic Edematous Response of the Human Heart to Myocardial Infarction: Implications for Assessing Myocardial Area at Risk and Salvage”

Multiparametric CMR imaging of infarct remodeling in a percutaneous reperfused Yucatan mini‐pig model

Measuring Water Distribution in the Heart: Preventing Edema Reduces Ischemia–Reperfusion Injury

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