Delayed hyperenhancement patterns in occlusive and reperfused myocardial infarcts during different healing stages

Wang, Yi; Sun, Wei; Cao, Guang; Meng, Lei; Song, Li; Xiang-ke, DU

doi:10.1002/jmri.20710

Cited by 11 publications

(20 citation statements)

References 19 publications

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“…There were not differences in time to peak (time interval between preinjection and the peak of bolus injection) between scarred and normal myocardium. No perfusion defect was detected on first-pass MRI in 4-week-old scar infarction, which is consistent with prior study demonstrating that the first-pass perfusion defect is detected 4 hours after permanent coronary occlusion and the perfusion defect disappeared 8 days afterwards [13]. These provide strong evidences that two types of CAs can be effectively delivered into scarred myocardium.…”

Section: Discussionsupporting

confidence: 91%

Pathological Mechanism for Delayed Hyperenhancement of Chronic Scarred Myocardium in Contrast Agent Enhanced Magnetic Resonance Imaging

et al. 2014

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ObjectivesTo evaluate possible mechanism for delayed hyperenhancement of scarred myocardium by investigating the relationship of contrast agent (CA) first pass and delayed enhancement patterns with histopathological changes.Materials and MethodsEighteen pigs underwent 4 weeks ligation of 1 or 2 diagonal coronary arteries to induce chronic infarction. The hearts were then removed and perfused in a Langendorff apparatus. The hearts firstly experienced phosphorus 31 MR spectroscopy. The hearts in group I (n = 9) and II (n = 9) then received the bolus injection of Gadolinium diethylenetriamine pentaacetic acid (0.05 mmol/kg) and gadolinium-based macromolecular agent (P792, 15 µmol/kg), respectively. First pass T2 * MRI was acquired using a gradient echo sequence. Delayed enhanced T1 MRI was acquired with an inversion recovery sequence. Masson's trichrome and anti- von Willebrand Factor (vWF) staining were performed for infarct characterization.ResultsWash-in of both kinds of CA caused the sharp and dramatic T2 * signal decrease of scarred myocardium similar to that of normal myocardium. Myocardial blood flow and microvessel density were significantly recovered in 4-week-old scar tissue. Steady state distribution volume (ΔR1 relaxation rate) of Gd-DTPA was markedly higher in scarred myocardium than in normal myocardium, whereas ΔR1 relaxation rate of P792 did not differ significantly between scarred and normal myocardium. The ratio of extracellular volume to the total water volume was significantly greater in scarred myocardium than in normal myocardium. Scarred myocardium contained massive residual capillaries and dilated vessels. Histological stains indicated the extensively discrete matrix deposition and lack of cellular structure in scarred myocardium.ConclusionsCollateral circulation formation and residual vessel effectively delivered CA into scarred myocardium. However, residual vessel without abnormal hyperpermeability allowed Gd-DTPA rather than P792 to penetrate into extravascular compartment. Discrete collagen fiber meshwork and loss of cellularity enlarged extracellular space accessible to Gd-DTPA, resulting in the delayed hyper-enhanced scar.

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Section: Discussionsupporting

confidence: 91%

Pathological Mechanism for Delayed Hyperenhancement of Chronic Scarred Myocardium in Contrast Agent Enhanced Magnetic Resonance Imaging

et al. 2014

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“…After 8 weeks, there was an excellent agreement between LE and TTC staining. Further data reported LE results for an ischemic time of 90 min being comparable to the LE in group B of the present study [51] . Likewise, the areas of microvascular obstruction decreased in size over time [51] , which was dependent on ischemic time and size of myocardial infarction as seen in previous pharmacological studies [5] .…”

Section: Discussionsupporting

confidence: 68%

“…Further data reported LE results for an ischemic time of 90 min being comparable to the LE in group B of the present study [51] . Likewise, the areas of microvascular obstruction decreased in size over time [51] , which was dependent on ischemic time and size of myocardial infarction as seen in previous pharmacological studies [5] . Microvascular obstruction itself assessed by ceCMRI is clinically of prognostic importance [52][53][54] .…”

Section: Discussionsupporting

confidence: 68%

Area at Risk and Viability after Myocardial Ischemia and Reperfusion Can Be Determined by Contrast-Enhanced Cardiac Magnetic Resonance Imaging

Vosseler¹,

Abegunewardene²,

Hoffmann³

et al. 2009

Eur Surg Res

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Background/Aims: Clinical differentiation between infarcted and viable myocardium in the ischemic area at risk is controversial. We investigated the potential of contrast-enhanced cardiac magnetic resonance imaging (ceCMRI) in determining the area at risk 24 h after ischemia. Methods: Myocardial ischemia was induced by percutaneous coronary intervention of the left anterior descending coronary artery in pigs. Coronary occlusion time was 30 min in group A, which caused little myocardial infarction and 45 min in group B, which led to irreversible damage. 24 h after reperfusion ceCMRI was performed at 2 and 15 min after administration of gadolinium-diethylenetriamine pentaacetic acid. The area at risk was determined by intravenous injection of Evans blue and myocardial viability by triphenyltetrazolium-chloride staining. Results: The signal-intense areas at 2 and 15 min after contrast administration matched the area at risk in groups A and B. Nonviable myocardium in group A was overestimated (14–15%) while good agreement was present in group B. Conclusion: The area at risk of reperfused ischemic myocardium can be determined by ceCMRI 24 h after coronary recanalization. This type of information might have relevant clinical implications in the treatment and stratification of patients with acute coronary syndrome in particular after surgical interventions.

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“…Lee et al have demonstrated that myocardial ischemia caused by the occlusion of a cat coronary artery is hypoenhanced relative to the normal myocardium [22] . Wang et al demonstrated that the nonreperfused occlusive infarct exhibits a first-pass perfusion defect without any delayed hyperenhancement at 4 h after coronary occlusion [23] . Thus, the disappearance of delayed Figure 4.…”

Section: Discussionmentioning

confidence: 99%

Collateral circulation formation determines the characteristic profiles of contrast-enhanced MRI in the infarcted myocardium of pigs

et al. 2015

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Aim: To investigate the relationship between the collateral circulation and contrast-enhanced MR signal change for myocardial infarction (MI) in pigs. Methods: Pigs underwent permanent ligation of two diagonal branches of the left anterior descending artery. First-pass perfusion (FPP) MRI (for detecting myocardial perfusion abnormalities) and delayed enhancement (DE) MRI (for estimating myocardial infarction) using Gd-DTPA were performed at 2 h, 7 d and 4 weeks after the coronary occlusion. Myocardial blood flow (MBF) was evaluated using nonradioactive red-colored microspheres. Histological examination was performed to characterize the infarcts. Results: Acute MI performed at 2 h afterwards was characterized by hypoenhancement in both FPP-and DE-MRI, with small and almost unchanged FPP-signal intensity (SI) and DE-SI due to negligible MBF. Subacute MI detected 7 d afterwards showed small but significantly increaseing FPP-SI, and was visible as a sluggish hyperenhancement in DE-MRI with considerably higher DE-SI compared to the normal myocardium; the MBF approached the half-normal value. Chronic MI detected at 4 weeks afterwards showed increasing FPP-SI comparable to the normal myocardium, and a rapid hyperenhancement in DE-MRI with even higher DE-SI; the MBF was close to the normal value. The MBF was correlated with FPP-SI (r=+0.94, P<0.01) and with the peak DE-SI (r=+0.92, P<0.01) at the three MI stages. Remodeled vessels were observed at intra-infarction and peri-infarction zones during the subacute and chronic periods. Conclusion: Progressive collateral recovery determines the characteristic profiles of contrast-enhanced MRI in acute, subacute and chronic myocardial infarction in pigs. The FPP-and DE-MRI signal profiles not only depend on the loss of tissue viability and enlarged interstitial space, but also on establishing a collateral circulation.

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Delayed hyperenhancement patterns in occlusive and reperfused myocardial infarcts during different healing stages

Cited by 11 publications

References 19 publications

Pathological Mechanism for Delayed Hyperenhancement of Chronic Scarred Myocardium in Contrast Agent Enhanced Magnetic Resonance Imaging

Pathological Mechanism for Delayed Hyperenhancement of Chronic Scarred Myocardium in Contrast Agent Enhanced Magnetic Resonance Imaging

Area at Risk and Viability after Myocardial Ischemia and Reperfusion Can Be Determined by Contrast-Enhanced Cardiac Magnetic Resonance Imaging

Collateral circulation formation determines the characteristic profiles of contrast-enhanced MRI in the infarcted myocardium of pigs

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