Infarct Edema Research Articles

Correlation of greyzone fibrosis compared to troponin T and late gadolinium enhancement with survival and ejection fraction in patients after acute myocardial infarction.

To quantify greyzone fibrosis (GZF) in patients after acute myocardial infarction (MI) and to evaluate its correlation with MI-free survival and improvements in left ventricular ejection fraction (LVEF) compared with the established risk factors high-sensitivity cardiac troponin T (hs-cTnT) and Late Gadolinium Enhancement (LGE). The study involved 176 patients who experienced acute MI and underwent cardiac magnetic resonance (CMR) prior to hospital discharge, followed by a second CMR on average six months later. LGE was quantified in both examinations, a separate analysis of the GZF was conducted only in the follow-up CMR after resolution of the initial infarct edema. LVEF was measured in both CMR. hs-cTnT levels were assessed at hospital admission, as well as 8, 16, 24, 48 and 72h after coronary intervention. Telephone follow-ups were conducted annually for up to 8years. LGE measurements showed better correlation with MI-free survival (Harrell's C of 0.711 of LGE mass) compared to GZF (0.579 of GZF mass). Additionally, hs-cTnT outperformed GZF (Harrell's C of 0.645). As an univariable predictor for MI-free survival, only hs-cTnT reached significance (p < 0.05). With regard to improvements in ejection fraction, both hs-cTnT and LGE measurements showed acceptable correlation with improvement in ejection fraction (p < 0.05), while GZF measurements showed no correlation (p > 0.5). In CMR, the assessment of GZF demonstrated inferior p correlation compared to hs-cTnT and LGE in patients after acute MI with respect to the endpoint of MI-free survival. Furthermore, GZF showed no correlation with the improvement of LVEF.

Rate of Infarct–Edema Growth on CT Predicts Need for Surgical Intervention and Clinical Outcome in Patients with Cerebellar Infarction

BackgroundUp to 20% of patients with cerebellar infarcts will develop malignant edema and deteriorate clinically. Radiologic measures, such as initial infarct size, aid in identifying individuals at risk. Studies of anterior circulation stroke suggest that mapping early edema formation improves the ability to predict deterioration; however, the kinetics of edema in the posterior fossa have not been well characterized. We hypothesized that faster edema growth within the first hours after acute cerebellar stroke would be an indicator for individuals requiring surgical intervention and those with worse neurological outcomes.MethodsConsecutive patients admitted to the neurological intensive care unit with acute cerebellar infarction were retrospectively identified. Hypodense regions of infarct and associated edema, “infarct–edema”, were delineated by using ABC/2 for all computed tomography (CT) scans up to 14 days from last known well. To examine how rate of infarct–edema growth varied across clinical variables and surgical intervention status, nonlinear and linear mixed-effect models were performed over 2 weeks and 2 days, respectively. In patients with at least two CT scans, multivariable logistic regression examined clinical and radiological predictors of surgical intervention (defined as extraventricular drainage and/or posterior fossa decompression) and poor clinical outcome (discharge to skilled nursing facility, long-term acute care facility, hospice, or morgue).ResultsOf 150 patients with acute cerebellar infarction, 38 (25%) received surgical intervention and 45 (30%) had poor clinical outcome. Age, admission National Institutes of Health Stroke Scale (NIHSS) score, and baseline infarct–edema volume did not differ, but bilateral/multiple vascular territory involvement was more frequent (87% vs. 50%, p < 0.001) in the surgical group than that in the medical intervention group. On 410 serial CTs, infarct–edema volume progressed rapidly over the first 2 days, followed by a subsequent plateau. Of 112 patients who presented within two days, infarct–edema growth rate was greater in the surgical group (20.1 ml/day vs. 8.01 ml/day, p = 0.002). Of 67 patients with at least two scans, after adjusting for baseline infarct–edema volume, vascular territory, and NIHSS, infarct–edema growth rate over the first 2 days (odds ratio 2.55; 95% confidence interval 1.40–4.65) was an independent, and the strongest, predictor of surgical intervention. Further, early infarct–edema growth rate predicted poor clinical outcome (odds ratio 2.20; 95% confidence interval 1.30–3.71), independent of baseline infarct–edema volume, brainstem infarct, and NIHSS.ConclusionsEarly infarct–edema growth rate, measured via ABC/2, is a promising biomarker for identifying the need for surgical intervention in patients with acute cerebellar infarction. Additionally, it may be used to facilitate discussions regarding patient prognosis.

Cardiac MRI: T2-Mapping Versus T2-Weighted Dark-Blood TSE Imaging for Myocardial Edema Visualization in Acute Myocardial Infarction

To assess the diagnostic accuracy of T2 mapping for the detection of myocardial edema in acute myocardial infarction (AMI), and to compare this diagnostic accuracy with that of the current standard for myocardial edema imaging, which is T2w dark-blood TSE imaging. 29 patients with AMI were examined at 1.5 T. For the visualization of myocardial edema, T2 maps, calculated from three T2w SSFP images, and T2w dark-blood TSE images were acquired in standard short- and long-axis views. Cine SSFP images were acquired for the analysis of left ventricular (LV) function and late gadolinium enhancement images (LGE) for the visualization of myocardial necrosis. The T2 maps as well as the T2w dark-blood TSE images were evaluated twice independently from the cine SSFP and LGE images. The presence or absence of myocardial edema was rated visually for each LV segment. As the standard of reference, the infarct zone was defined based on the cine SSFP and the LGE images. In this segment-based analysis, T2 mapping showed a sensitivity of 82 % and a specificity of 94 % for the detection of edema in the infarct zone. T2w dark-blood TSE imaging revealed a sensitivity of 50 % and a specificity of 98 %. T2 mapping showed a higher intra-rater agreement compared to T2w dark-blood TSE imaging (κ: 0.87 vs. 0.76). T2 mapping allows for the visualization of myocardial edema in AMI with a high sensitivity and specificity, and features better diagnostic accuracy in terms of a higher sensitivity compared to T2w dark-blood TSE imaging. Citation Format: • Naßenstein K, Nensa F, Schlosser T et al. Cardiac MRI: T2-Mapping Versus T2-Weighted Dark-Blood TSE Imaging for Myocardial Edema Visualization in Acute Myocardial Infarction. Fortschr Röntgenstr 2014; 186: 166 - 172.

Quantitative T2 mapping for detecting myocardial edema after reperfusion of myocardial infarction: validation and comparison with T2-weighted images

This study evaluates the clinical usefulness of T2 mapping for the detection of myocardial edema in the re-perfused acute myocardial infarction (MI). Cardiac MRIs were reviewed in 20 patients who had acute MI after reperfusion therapy. The regional T2 values and T2-weighted image (T2WI) signal intensities (SI) were measured in the infarcted and remote zones of the myocardium. Patients were divided into three groups according to the signal patterns of the infarcted myocardium on the T2WIs. The T2 values of the infarcted zones were compared on the T2 maps among the three groups. Validation of the T2 values was performed in the normal myocardium of seven healthy volunteers. There were no significant differences in mean T2WI-SI or T2 values in the normal myocardium of healthy volunteers compared to the remote myocardium of acute MI patients (p > 0.05). Mean SI on the T2WIs was significantly higher in the infarcted myocardium (81.3 ± 37.6) than in the remote myocardium (63.8 ± 18.1) (p < 0.05). The T2WIs showed high SI in ten patients (group 1), iso-SI in seven (group 2), and low SI in three (group 3) in the infarcted myocardium, compared to the remote myocardium. The T2 maps showed that T2 values in the infarcted myocardium had mostly increased, regardless of group, with values of 71 ± 9 ms in group 1, 64.9 ± 7.4 ms in group 2, and 61.4 ± 8.5 ms in group 3. T2 mapping is superior to T2WI for detecting areas of high SI in the infarcted myocardium. Therefore, quantitative T2 mapping sequences may be more useful and reliable in identifying myocardial edema in the infarcted myocardium than T2WI.

Diabetes is associated with increased and persistent myocardial edema in infarct segment post acute myocardial infarction

Summary Our study demonstrates that diabetic patients have increased myocardial edema in the infarct segment at an early time point post acute myocardial infarction which persists till the subacute phase. This may lead to deleterious left ventricular remodeling and worse outcome in these patients. Background Diabetes is associated with worse left ventricular remodeling and poor prognosis in patients post acute myocardial infarction (AMI). The impact of diabetes on microvascular injury parameters including myocardial edema and hemorrhage post AMI is unknown. Our objective was to characterize the evolution of myocardial edema and hemorrhage post AMI in patients with and without diabetes. Methods Sixty patients were enrolled post AMI and underwent cardiac magnetic resonance on a GE Signa Excite, 1.5T scanner with a 8-channel receive coil at 48 hours and 3 weeks. T2 maps were computed from a previously validated cardiac-gated spiral imaging sequence with T2 preparations yielding TEs=2.9,24.3,88.2,184.2ms to assess myocardial edema. The T2* sequence was a multiecho acquisition with 8 echoes (between 1.4 and 12.7ms) acquired at TR=14.6ms. Delayed hyperenhancement was also performed. We retrospectively reviewed and stratified patients into those that did and did not have diabetes (type 1 or type 2). Results We compared 15 diabetics versus 45 non-diabetics (Table 1). Baseline characteristics including age, gender, symptom to balloon time, door to balloon time, glycoprotein IIb/IIIa inhibitor use, and thrombus aspiration use were similar in both groups. The mean T2 was higher in the infarct segment (IS) compared to remote segment (RS) in both patient groups (diabetics: 59.3ms vs 41.3ms, p<0.0001 vs non-diabetics: 52.9ms vs 40.1ms, p<0.0001). The mean T2* was similar in the IS compared to RS in both diabetics (32.1ms vs 38.0ms; p=0.11) and non-diabetics (33.9ms vs 36.7ms; p=0.09). The mean T2 was significantly higher in the IS of diabetic patients versus non-diabetics (59.3ms vs 52.9ms; p=0.03). The mean T2* was equivalent in the IS of both patient groups (32.1ms vs 33.9ms; p=0.59).

Selective MMP-inhibition with Ro 28-2653 in acute experimental stroke – a magnetic resonance imaging efficacy study

Blood–brain-barrier (BBB) breakdown due to matrix metalloproteinase (MMP) activity following stroke is often associated with cerebral edema, larger infarct volumes and bad outcome. In the present study we examined a novel MMP-inhibitor (Ro 28-2653) with high selectivity for MMP2, MMP9 and membrane type 1-MMP in an acute stroke model comparing two different treatment regimens. We subjected rats to 90 min of focal cerebral ischemia followed by 3 days or 7 days of reperfusion, respectively, using the middle cerebral artery (MCA) filament occlusion technique. Ro 28-2653 was administered daily in a vehicle solution for 2 days or 6 days after ischemia, respectively. We assessed the behavior with a functional neuroscore and infarct volumes as well as blood–brain-barrier (BBB) breakdown with magnetic resonance imaging (MRI) after 3 and 7 days. Infarct edema volumes, BBB breakdown and behavior at 3 days were significantly attenuated in rats treated for 2 days with Ro 28-2653 as compared to vehicle and untreated controls. After 6 days of treatment however, infarct and BBB breakdown volumes as well as behavior did not differ significantly between the groups at 7 days. The new high selective MMP-inhibitor Ro 28-2653 significantly reduced brain injury only when administered in the first 2 days after focal cerebral ischemia. Prolonged treatment for 6 days did not show any beneficial effects possibly due to interference with protective restorative processes.

MRI Restricted Diffusion in Optic Nerve Infarction After Autologous Fat Transplantation

A 24-year-old woman reported blindness in the left eye upon awakening from fat autotransplantation to her forehead for soft tissue augmentation in the face. Clinical findings on the third postoperative day suggested ipsilateral ophthalmic artery occlusion with infarction of the optic nerve and retina. There were also clinical manifestations of a mild right hemiparesis. MRI diffusion-weighted imaging (DWI) revealed restricted diffusion of the left optic nerve and left middle cerebral artery domain indicative of the cytotoxic edema of infarction. This is the second report of optic nerve infarction after fat autotransplantation to the forehead and the first report of DWI restricted diffusion in this setting.

Intra-Arterial Iodinated Radiographic Contrast Material Injection Administration in a Rat Middle Cerebral Artery Occlusion and Reperfusion Model

Observations in human interventional stroke treatment led us to hypothesize that iodinated radiographic contrast material use may contribute to intracerebral hemorrhage. Effects of intra-arterial iodinated radiographic contrast material on hemorrhagic transformation after middle cerebral artery occlusion and reperfusion were studied in a placebo-controlled, blinded preclinical study in rats. Four groups of male Sprague-Dawley rats were studied: saline group (n=8), contrast group (n=12), heparin group (n=9), and contrast+heparin group (n=9). The middle cerebral artery was occluded for 5 hours using suture placement. Heparin was infused before suture removal and reperfusion. Saline and/or contrast were infused immediately during reperfusion. Incidence, location, and size of hemorrhage were determined by brain necropsy inspection at 24 hours. There was a significant increase in incidence of cortical hemorrhage from control (37.5%), contrast (75.0%), heparin (77.8%) to contrast+heparin (100%; Cochran-Mantel-Haenszel correlation, P<0.01). Both pooled contrast groups (85.7%) and pooled heparin groups (88.9%) had higher rates of cortical intracerebral hemorrhage compared with the control group (P<0.05). Similar trends for increased cortical intracerebral hemorrhage were seen in the contrast-only (P=0.18) and heparin-only (P=0.18) groups. There was a trend for decreased infarct edema in rats receiving contrast versus those without (P=0.06). Intraarterial iodinated radiographic contrast material may increase cortical intracerebral hemorrhage, similar to heparin. Iodinated radiographic contrast material effect may be additive to heparin effect on the incidence of cortical intracerebral hemorrhage.

Abstract 3418: Infarct-Related Myocardial Edema Detected by Diffusion-Weighted Imaging; Comparison with T2-Weighted imaging

Background: Cardiac MRI permits diagnosis with acute myocardial infarction (AMI) by detection of infarct-related myocardial edema (IRME) on black-blood T2-weighted images (T2WIs), and myocardial scar on delayed-enhanced images (DEs). Diffusion-weighted image (DWI) is an established method for detection of cerebral infarction edema, but few reports are available on detection of IRME. Objective: To detect IRME using DWIs, and compare the contrast-to-noise ratio (CNR) with T2WIs. Methods: Cardiac MRI was performed on a 1.5T scanner (SIEMENS Avanto, Erlangen, Germany) in 12 AMI patients within 14 days after successful reperfusion. T2WIs were acquired using a double inversion-recovery fast-spin echo sequence. DWIs were acquired using combined cardiac and respiratory gated single-shot echo-planar sequence with a b-value of 50 s/mm 2 . DEs were acquired using an inversion-recovery segmented gradient-echo sequence, fifteen minutes after administering 0.15 mmol/kg gadolinium-DTPA. CNR was calculated in the T2WIs and DWIs using the following formula: CNR = (signal intensity[ME]-signal intensity[M]) / SD(B), where ME = myocardial edema, M = myocardium, and SD(B) =standard deviation of background signal intensity. Results: IRME was detected on T2WIs, and myocardial scar on DEs in all patients. DWIs revealed an area of significantly increased signal intensity in the same region identified as IRME on T2WIs in all patients. The CNR of DWIs (78.9 ± 44.5) was significantly higher than those of T2WIs (31.5 ± 23.3) (p = 0.0001). Conclusion: Our findings indicate that low b-value DWI provides better contrast in infarct-related myocardial edema than T2WIs.

Clinical application of diffusion-weighted magnetic resonance imaging to intracranial disorders.

Diffusion-weighted magnetic resonance imaging was performed to determine the changes in water diffusion and to investigate the detectability of diffusion anisotropy in patients with intracranial disorders. Diffusion maps of the apparent diffusion coefficient (ADC) were created of 19 patients with cerebral infarction, five with intracerebral hematoma, four with glioma, four with meningioma, four with hydrocephalus, and five with subdural hematoma. ADC was increased in chronic cerebral infarction and glioma, and decreased in acute cerebral infarction, meningioma, and the marginal area of glioma compared with the ADC of the normal gray matter. There was a significant difference in ADC between the marginal and internal areas of glioma. Increased ADC may be due to increased vasogenic edema in infarction and a lack of significant restriction of diffusion within glioma. Decreased ADC can be attributed to restricted diffusion caused by cytotoxic edema in infarction and the underlying histological pattern of densely packed tumor cells in glioma. Diffusion anisotropy of the internal capsule was less detectable in pathological than normal hemispheres. Diffusion anisotropy was less detectable in patients with hydrocephalus and subdural hematoma. Intracranial lesions were thought to have influenced the compression of the brain structures and cells, resulting in decreased diffusion. The measurement of ADC by diffusion-weighted magnetic resonance imaging has the potential for greater understanding of the biophysical changes in various intracranial disorders, including correct diagnosis of cerebral infraction, and histological diagnosis of brain tumor.

Subcortical U-fibers layer preservation in brain edema.

The mechanism involved in the relative preservation of the subcortical U-fibers in the arcuate zone was studied in a post infarct edema after sagittal superior sinus occlusion. Superior sagittal sinus (SSS) of 36 mongrel cats were occluded by polymer injection. Immediately before the occlusion Evans-blue (EB) was administered intravenously. The cats were killed 1, 2, 3, 6, 12, 24, 72 and 120 hours after sinus occlusion. In 20 cats in which cortical veins were occluded, in addition to the SSS, EB was extravasated. In 9 of these cats, which had moderate edema, EB-staining was present only in the cortex. In 11 cats with severe edema, massive EB extravasation was observed also in the white matter. The U-fiber layer was free of EB, suggesting that the extension of edema was blocked by this zone. Our findings demonstrated that the U-fibers act not only as a resistance against extension of edema from white to gray matter, but also in a reverse direction. The characteristics of the spread of brain edema is not yet completely understood; both anatomical and biochemical peculiarities from its basis. Different morphological patterns in the astrocytic reaction as well as the U-fibers sector vascularization are important. To evaluate the role of each one of these factors in the preservation of subcortical U-fiber layer in brain edema further investigations should be done.

Hemorrhagic transformation in cardioembolic cerebral infarction.

Because the frequency of hemorrhagic transformation of cerebral infarcts is still a matter of controversy, we performed a prospective magnetic resonance imaging study in a series of consecutive patients with cardioembolic stroke. Among 200 consecutive patients with transient ischemic attack or ischemic stroke, 41 were identified with a computed tomographically proven supratentorial infarct due to cardiogenic embolism. Magnetic resonance imaging (T1-weighted) was performed 3 weeks after the stroke in 35 of these 41 patients. Eight patients received anticoagulants. Magnetic resonance images showed hemorrhagic transformation in 68.6% (24) of the 35 infarcts, always without clinical deterioration. In a stepwise forward logistic regression analysis only the volume of infarction edema on the initial computed tomogram was linked significantly with the risk of hemorrhagic transformation (p = 0.037). Hemorrhages were a regular finding on magnetic resonance images of infarcts exceeding a volume of 10 cm3 (94.4%, 17 of 18). Hemorrhagic transformation is a regular finding in medium-sized and large cardioembolic infarcts. Thus, in therapeutic and preventive studies of acute stroke the severity, not the frequency, of hemorrhages into brain infarcts should be the matter of interest.

Accumulation of hyaluronan and tissue edema in experimental myocardial infarction.

Experimental myocardial infarction was induced in rats. The myocardial accumulation of hyaluronan (HA) and water during the development of infarction was measured. The extractable HA content of the infarcted area increased progressively from day 1 and on day 3 reached a threefold increase compared with the HA amounts in myocardium of sham operated controls. The relative water content of infarcted areas also increased progressively reaching a maximum value by day 3 and was strongly correlated with the HA accumulation. Affinity histochemistry visualized a thin rim of HA in the endoperimysium in healthy myocardium. By day 2 an interstitial edema with inflammatory cells was apparent. The widened endoperimysium stained extensively for HA. By its water-binding ability, interstitial accumulation of HA will contribute to the interstitial edema in infarcted myocardial tissue. An interstitial edema is likely to influence the electromechanical characteristics of the myocardium and facilitate reentry phenomena due to a loss of contact between muscle cells. The edema also induces an increased extracellular pressure and an altered myocardial wall compliance that might impair myocardial microcirculation. The findings are relevant to an understanding of the beneficial effect of hyaluronidase treatment in limiting cellular damage during myocardial ischemia.

The measurement of cerebral infarction edema with sodium 22.

Sodium 22 was used to determine quantitatively cerebral infarction edema in cats after occlusion of the middle cerebral artery. A comparison was made of the sodium 22 edema determination with the wet weight-dry weight method of edema determination. There was a high degree of correlation between the two methods. The sodium 22 method of measuring cerebral infarction edema was less time consuming and easier than the wet weight-dry weight method, and served as a reliable means of quantitatively comparing the edema content in the hemispheres of animals with stroke.