Physiological Basis of Myocardial Contrast Enhancement in Fast Magnetic Resonance Images of 2-Day-Old Reperfused Canine Infarcts

Judd, Robert M.; Lugo-Olivieri, Carlos H.; Arai, M.; Kondo, Takeshi; Croisille, Pierre; Lima, João A.C.; Mohan, Vivek; Becker, Lewis C.; Zerhouni, Elias A.

doi:10.1161/01.cir.92.7.1902

Cited by 412 publications

(305 citation statements)

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“…However, this notion of a confinement of no-reflow to infarcted myocardium is based on experimental studies with mechanical occlusion and reperfusion of virgin coronary arteries or clinical studies using MRI several days after established reperfusion. In such experimental studies, coronary microembolization with subsequent microinfarcts into not grossly infarcted myocardium of the area at risk does not occur, and in such clinical studies using MRI coronary microembolization might occur but not be detected, as MRI identifies no-reflow areas as areas of hypoenhancement within areas of hyperenhancement, i.e., grossly infarcted myocardium [11,23]. Microinfarction after microembolization is only detected by MRI when affecting more than 5 % of myocardium [18].…”

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confidence: 99%

Myocardial infarction and coronary microvascular obstruction: an intimate, but complicated relationship

2013

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Timely reperfusion is the only way to rescue ischemic myocardium from impending infarction. However, reperfusion also adds a component of injury to that incurred during ischemia and thus contributes to final infarct size [6,20,28]. It appears that all conditioning strategies which delay infarct size development and/or reduce infarct size act through attenuation of such reperfusion injury [7]. Apart from its contribution to cardiomyocyte necrosis, reperfusion is frequently also characterized by the development of areas of no-reflow within the previously ischemic myocardium [10]. Evidence for microvascular no-reflow by angiography or MRI despite successfully reopened epicardial coronary arteries in patients with myocardial infarction is associated with impaired recovery of ventricular function and worse survival [19].The coexistence of infarcted cardiomyocytes and areas of coronary microvascular no-reflow in reperfused myocardium is well established [13]; however the underlying mechanisms are not really clear. Several mechanisms can initiate no-reflow in previously ischemic myocardium: (a) embolization of particulate atherosclerotic debris from the culprit lesion into the coronary microcirculation, both after mechanical or thrombolytic reopening of epicardial coronary arteries The analysis of temporal and spatial relationships between infarcted myocardium and no-reflow is largely limited by methodological restraints. By definition, infarcted myocardium and no-reflow are confined to the previously ischemic area at risk. This appears trivial, but when analyzed by clinical imaging technology, the area at risk is often not determined or not clear. Slow/no-flow phenomena outside the area at risk may also occur but have a different underlying pathophysiology, e.g., reflex-mediated coronary vasoconstriction [4,8]. Myocardial infarction develops progressively during ischemia, and a separate component of irreversible injury is added during early reperfusion; the relative contribution of infarction which develops during ischemia and during reperfusion varies and depends on the duration of ischemia [3]. Even with gold standard technology (TTC staining) in the experiment, infarcted tissue is only recognized as such after several hours of reperfusion, and no distinction between myocardium infarcting during ischemia and during reperfusion is possible. No-reflow, as evidenced by lack of endothelial staining by thioflavin in the experiment [13], develops rapidly during early reperfusion and progresses over time [1,22,23]. Most studies indicate that no-reflow areas are This comment refers to the article available at

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confidence: 99%

Myocardial infarction and coronary microvascular obstruction: an intimate, but complicated relationship

2013

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“…[5][6][7][8][9][10][11][12][13][14] Extracellular MR contrast media such as Gd-DTPA are passively distributed into the interstitium from intact capillaries in normal myocardium. Disruption of cellular membrane, expansion of interstitium, and increased blood volume provide an expanded distribution volume for these agents.…”

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confidence: 99%

Magnetic Resonance Characterization of the Peri-Infarction Zone of Reperfused Myocardial Infarction With Necrosis-Specific and Extracellular Nonspecific Contrast Media

et al. 2001

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Background-Because ischemically injured myocardium is frequently composed of viable and nonviable portions, a method to discriminate the two is useful for clinical management. Methods and Results-Ischemically injured myocardium was characterized with extracellular nonspecific (Gd-DTPA) and necrosis-specific (mesoporphyrin) MR contrast media in rats. Relaxation rates (R1) were measured on day 1 and day 2 by inversion-recovery echoplanar imaging. Spin-echo imaging was used to define contrast-enhanced regions and regional wall thickening. Gadolinium concentration, area at risk, and infarct size were measured at postmortem examination. ⌬R1 ratio (⌬R1 myocardium /⌬R1 blood ) after administration of Gd-DTPA was greater in ischemically injured myocardium (1.20Ϯ0.15) than in normal myocardium (0.47Ϯ0.05, PϽ0.05), which was attributed to differences in gadolinium concentration and water content. The Gd-DTPA-enhanced region on day 2 was larger (32.8Ϯ0.9%) than true infarction as demonstrated by triphenyltetrazolium chloride (TTC) (24.6Ϯ1.4%, PϽ0.001, rϭ0.21). Bland-Altman analysis revealed that the Gd-DTPA-enhanced region overestimated true infarct size by 7.8Ϯ5.9%. On the other hand, the mesoporphyrin-enhanced region (26.9Ϯ1.8%, PϭNS, rϭ0.87) and true infarct size were identical. The difference in the areas demarcated by the 2 agents is the peri-infarction. Systolic and diastolic MR images revealed no wall thickening in the mesoporphyrin-enhanced region (0.3Ϯ3.3%) but reduced thickening in the Gd-DTPA-enhanced rim (8.5Ϯ5.5%, PϽ0.05). Conclusions-The Gd-DTPA-enhanced region encompasses both viable and nonviable portions of the ischemically injured myocardium. The Gd-DTPA-enhanced area overestimated infarct size, but the mesoporphyrin-enhanced area matched true infarct size. The salvageable peri-infarction zone can be characterized with double-contrast-enhanced and functional MR imaging; the mismatched area of enhancement between the 2 agents shows residual wall thickening.

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“…PIS PIM ϭ 100 ⅐ IMS PIM / m slice [6] where m slice was the mass of the slice obtained by summing all voxel masses in the slice. TIM PIM was calculated by summing IMS PIM from all SAX slices plus the apex.…”

Section: Pim Image Processingmentioning

confidence: 99%

“…Several investigators have found that in ceMRI, ie, MRI enhanced typically with a gadolinium (Gd)-based contrast agent (CA), a signal enhancement of myocardial tissue occurs in acutely reperfused infarcts (4,5). This enhancement starts a few hours after cellular damage but still occurs even on the second day of infarct (6), and can be observed even in the healed phase of myocardial infarction (7).…”

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confidence: 99%

Head‐to‐head comparison between delayed enhancement and percent infarct mapping for assessment of myocardial infarct size in a canine model

Ruzsics

Surányi

Kiss

et al. 2008

Magnetic Resonance Imaging

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Purpose: To compare a novel method, percent-infarctmapping (PIM), with conventional delayed enhancement (DE) of contrast for accurate myocardial viability assessment. Contrary to signal intensity (SI), the longitudinal relaxation-rate enhancement (⌬R1) is an intrinsic parameter linearly proportional to the concentration of contrast agent (CA). Determining ⌬R1 voxel-by-voxel, after administering an infarct-avid CA, allows determination of pervoxel percentage of infarcted tissue. The feasibility of generating PIM is demonstrated in canine reperfused infarction using an infarct-avid, persistent-CA (PCA), (Gd)(ABE-DTTA). PIM is compared to the DE method using Gd(DTPA), and both to triphenyltetrazolium chloride (TTC) staining histochemistry. Materials and Methods:In six dogs, 48 hours following closed-chest, 180-minute coronary occlusion, DE imaging was carried out. PCA was administered immediately thereafter. Pixel-by-pixel R1 maps of the entire left ventricle (LV) were generated 48 hours after PCA using inversion-recovery with multiple inversion times. R1, ⌬R1, and percentinfarct values were calculated voxel-by-voxel.Results: Significant correlations (P Ͻ 0.01, R Ն 0.8) were obtained for percent-infarct-per-slice (PIS) determined by DE or PIM vs. those from corresponding TTC-stained slices. Compared to TTC, DE overestimated PIS by 32 Ϯ 18%. PIM underestimated PIS by 2.5 Ϯ 4.9%. Infarction fraction overestimation was 29 Ϯ 6% of LV by DE, but only 1.0 Ϯ 2.3% by PIM. Errors with PIM were significantly smaller than those with DE. Infarct area determined by signal intensity was similarly overestimated whether using Gd(DTPA) or Gd(ABE-DTTA). Conclusion:The ⌬R1-based PIM method is highly reproducible and more accurate than DE for quantifying myocardial viability in vivo.

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Physiological Basis of Myocardial Contrast Enhancement in Fast Magnetic Resonance Images of 2-Day-Old Reperfused Canine Infarcts

Abstract: In contrast-enhanced MR images of 2-day-old reperfused canine infarcts, myocardial regions of hypoenhancement are related to the no-reflow phenomenon. Approximately 90% of the myocardium within hyperenhanced regions is nonviable.

Cited by 412 publications

References 29 publications

Myocardial infarction and coronary microvascular obstruction: an intimate, but complicated relationship

Myocardial infarction and coronary microvascular obstruction: an intimate, but complicated relationship

Magnetic Resonance Characterization of the Peri-Infarction Zone of Reperfused Myocardial Infarction With Necrosis-Specific and Extracellular Nonspecific Contrast Media

Head‐to‐head comparison between delayed enhancement and percent infarct mapping for assessment of myocardial infarct size in a canine model

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