• The Korean Journal of Nuclear Medicine
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• v.25 no.1
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• pp.37-45
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• 1991

Infarct size is a major determinant of prognosis after acute myocardial infarction. Up to date, however, clinically available tests to estimate this size have not been sufficiently accurate. Twelve lead electrocardiogram and wall motion abnormality measurement are not quantitative, and creatine phophokinase (CPK) measurement is inaccurate in the presence of reperfusion or right ventricular infarction. Methods have been developed to localize and size acute myocardial infarcts with agents that are selectively sequestered in areas of myocardial damage, but previously used agents have lacked sufficient specificity. Antibodies that bind specifically only to damaged myocardial cells may resolve this problem and provide an accurate method for noninvasively measuring infarct size. We determined the accuracy with which infarcted myocardial mass can be measured using single photon emission computed tomography (SPECT) and radiolabeled antimyosin antibodies. Seven patients with acute myocardial infarction and one stable angina patient were injected with 2 mCi of Indium-111 labeled antimyosin antibodies. Planar image and SPECT was performed 24 hours later. None of the patients had history of prior infarcts, and none had undergone reperfusion techniques prior to the study, which was done within 4 days of the attack. Planar image showed all infarct patients to have postive uptakes in the cardiac region. The location of this uptake correlated to the infarct site as indicated by electrocardiography in most of the cases. The angina patient, however, showed no such abnormal uptake. Infarct size was determined from transverse slices of the SPECT image using a 45% threshold value obtained from a phantom study. Measured infarct size ranged from 40 to 192 gr. There was significant correlation between the infarct size measured by SPECT and that estimated from serial measurements of CPK (r=0.73, p<0.05). These date suggest that acute myocardial infarct size can be accurately measured from SPECT Indium-111 antimyosin imaging. This method may be especially valuable in situations where other methods are unreliable, such as early reperfusion technique, right ventricular infarct or presence of prior infarcts.

• Advances in biomechanics and applications
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• v.1 no.1
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• pp.41-55
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• 2014

Acellular intra-myocardial biomaterial injections have been shown to be therapeutically beneficial in inhibiting ventricular remodelling of myocardial infarction (MI). Based on a biventricular canine cardiac geometry, various finite element models were developed that comprised an ischemic (II) or scarred infarct (SDI) in left ventricular (LV) antero-apical region, without and with intra-myocardial biomaterial injectate in layered (L) and bulk (B) distribution. Changes in myocardial properties and LV geometry were implemented corresponding to infarct stage (tissue softening vs. stiffening, infarct thinning, and cavity dilation) and injectate (infarct thickening). The layered and bulk injectate increased ejection fraction of the infarcted LV by 77% (II+L) and 25% (II+B) at the ischemic stage and by 61% (SDI+L) and 63% (SDI+B) at the remodelling stage. The injectates decreased the mean end-systolic myofibre stress in the infarct by 99% (II+L), 97% (II+B), 70% (SDI+L) and 36% (SDI+B). The bulk injectate was slightly more effective in improving LV function at the remodelling stage whereas the layered injectate was superior in functional improvement at ischemic stage and in reduction of wall stress at ischemic and remodelling stage. These findings may stimulate and guide further research towards tailoring acellular biomaterial injectate therapies for MI.

• YAKHAK HOEJI
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• v.41 no.1
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• pp.117-125
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• 1997

The pharmacological effects of benzopyran potassium channel openers (lemakalim, KR-30450 and KR-30818) on the occlusion/reperfusion-induced myocardial infarction were investigat ed. In anesthetized rats, subjected to 45-min occlusion of the left anterior descending coronary artery (LAD) followed by 90-min reperfusion, the infarct size was measured by calculating the ratio of infarct zone to area at risk (IZ/AAR) with the Evans blue/TTC technique. Rats were intravenously given vehicle (1% DMSO), lemakalim, KR-30450, and KR-30818 alone or in combination with a selective K$_{ATP}$ blacker glibenclamide, 30 min prior to coronary occlusion. Compared to vehicle, lemakalim (30 ${\mu}$g/kg i.v.), the active enantiomer of cromakalim, had a tendancy to decrease infarct size. KR-30450(30 ${\mu}$g/kg, i.v.). the newly synthetized potassium channel openers (PCOs), caused a reduction of infarct size (from 70${\pm}$4%to 57${\pm}$5%). but KR-30818 (30 ${\mu}$g/kg, i.v.), a metabolite of KR-30450. did not modify infarct size. It seem ed likely that glibenclamide (0.3mg/kg, i.v.), given in combination, reduced the effects of these PCOs, especially KR-30450 (30 ${\mu}$g/kg, i.v.) on the infarct size. These results indicate that. in the coronary occluded rat model of ischemia, lemakalim and KR-30450 may exert cardioprotective activity through a reduction of infarct size, the effect being considered related to the opening of K$_{ATP}$ channel.

• Nutrition Research and Practice
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• v.8 no.4
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• pp.391-397
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• 2014

BACKGROUND/OBJECTIVE: Myocardial cell death due to occlusion of the coronary arteries leads to myocardial infarction, a subset of coronary heart disease (CHD). Dietary fiber is known to be associated with a reduced risk of CHD, the underlying mechanisms of which were suggested to delay the onset of occlusion by ameliorating risk factors. In this study, we tested a hypothesis that a beneficial role of dietary fiber could arise from protection of myocardial cells against ischemic injury, manifested after occlusion of the arteries. MATERIALS/METHODS: Three days after rats were fed apple pectin (AP) (with 10, 40, 100, and 400 mg/kg/day), myocardial ischemic injury was induced by 30 min-ligation of the left anterior descending coronary artery, followed by 3 hr-reperfusion. The area at risk and infarct area were evaluated using Evans blue dye and 2,3,5-triphenyltetrazolium chloride (TTC) staining, respectively. DNA nicks reflecting the extent of myocardial apoptosis were assessed by TUNEL assay. Levels of cleaved caspase-3, Bcl-2, and Bax were assessed by immunohistochemistry. RESULTS: Supplementation of AP (with 100 and 400 mg/kg/day) resulted in significantly attenuated infarct size (IS) (ratio of infarct area to area at risk) by 21.9 and 22.4%, respectively, in the AP-treated group, compared with that in the control group. This attenuation in IS showed correlation with improvement in biomarkers involved in the apoptotic cascades: reduction of apoptotic cells, inhibition of conversion of procaspase-3 to caspase-3, and increase of Bcl-2/Bax ratio, a determinant of cell fate. CONCLUSIONS: The findings indicate that supplementation of AP results in amelioration of myocardial infarction by inhibition of apoptosis. Thus, the current study suggests that intake of dietary fiber reduces the risk of CHD, not only by blocking steps leading to occlusion, but also by protecting against ischemic injury caused by occlusion of the arteries.

• International Journal of Stem Cells
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• v.17 no.1
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• pp.70-79
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• 2024

The efficacy of adipose-derived stem cells (ASCs) on myocardial infarction is limited due to poor survival and engraftment. Integrin-mediated cell adhesion is a prerequisite for its survival and homing. ASCs expressed insufficient integrin 𝛼₄, limiting their homing capacity. This study aims to characterize integrin 𝛼₄⁺ ASC subpopulation and investigate their therapeutic efficacy in myocardial infarction. We used fluorescence-activated cell sorting to harvest integrin 𝛼₄⁺ ASCs subpopulation, which were characterized in vitro and transplanted into myocardial infarction model. Positron emission tomography imaging were performed to measure infarction size. Cardiac cine magnetic resonance imaging was used to evaluate heart contractile function. Compared with the unfractionated ASCs, integrin 𝛼₄⁺ ASCs subpopulation secreted a higher level of angiogenic growth factors, migrated more rapidly, and exhibited a stronger anti-apoptotic capacity. Vascular cell adhesion molecule-1 was obviously up-regulated at 3 days after myocardial infarction, which interacted with integrin α₄ receptor on the surface of ASCs to enhance the survival and adhesion. Thus, we implanted unfractionated ASCs or integrin α₄⁺ ASCs subpopulation into the 3-day infarcted myocardium. Integrin α₄⁺ ASCs subpopulation exhibited more robust engraftment into the infarcted myocardium. Integrin α₄⁺ ASCs subpopulation more effectively decreased infarct size and strengthen cardiac function recovery than did the unfractionated ASCs. Integrin α₄⁺ ASCs subpopulation is superior to unfractionated ASCs in ameliorating ischemic myocardial damage in animal model. Mechanistically, their more robust engraftment into the infarct area, higher migratory capacity and their increased release of paracrine factors contribute to enhanced tissue repair.

• Korean Journal of Radiology
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• v.2 no.1
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• pp.21-27
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• 2001

Objective: To identify and evaluate the lateral border zone by comparing the size and distribution of the abnormal signal area demonstrated by MR imaging with the infarct area revealed by pathological examination in a reperfused myocardial infarction cat model. Materials and Methods: In eight cats, the left anterior descending coronary artery was occluded for 90 minutes, and this was followed by 90 minutes of reperfusion. ECG-triggered breath-hold turbo spin-echo T2-weighted MR images were initially obtained along the short axis of the heart before the administration of contrast media. After the injection of Gadomer-17 and Gadophrin-2, contrast-enhanced T1-weighted MR images were obtained for three hours. The size of the abnormal signal area seen on each image was compared with that of the infarct area after TTC staining. To assess ultrastructural changes in the myocardium at the infarct area, lateral border zone and normal myocardium, electron microscopic examination was performed. Results: The high signal area seen on T2-weighted images and the enhanced area seen on Gadomer-17-enhanced T1WI were larger than the enhanced area on Gadophrin-2-enhanced T1WI and the infarct area revealed by TTC staining; the difference was expressed as a percentage of the size of the total left ventricle mass (T2= 39.2 %; Gadomer-17 =37.25 % vs Gadophrin-2 = 29.6 %; TTC staining = 28.2 %; p < 0.05). The ultrastructural changes seen at the lateral border zone were compatible with reversible myocardial damage. Conclusion: In a reperfused myocardial infarction cat model, the presence and size of the lateral border zone can be determined by means of Gadomer-17- and Gadophrin-2-enhanced MR imaging.

• Progress in Medical Physics
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• v.22 no.1
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• pp.42-51
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• 2011

Nuclear medicine images (SPECT, PET) were widely used tool for assessment of myocardial viability and perfusion. However it had difficult to define accurate myocardial infarct region. The purpose of this study was to investigate methodological approach for automatic measurement of rat myocardial infarct size using polar map with adaptive threshold. Rat myocardial infarction model was induced by ligation of the left circumflex artery. PET images were obtained after intravenous injection of 37 MBq $^{18}F$-FDG. After 60 min uptake, each animal was scanned for 20 min with ECG gating. PET data were reconstructed using ordered subset expectation maximization (OSEM) 2D. To automatically make the myocardial contour and generate polar map, we used QGS software (Cedars-Sinai Medical Center). The reference infarct size was defined by infarction area percentage of the total left myocardium using TTC staining. We used three threshold methods (predefined threshold, Otsu and Multi Gaussian mixture model; MGMM). Predefined threshold method was commonly used in other studies. We applied threshold value form 10% to 90% in step of 10%. Otsu algorithm calculated threshold with the maximum between class variance. MGMM method estimated the distribution of image intensity using multiple Gaussian mixture models (MGMM2, ${\cdots}$ MGMM5) and calculated adaptive threshold. The infarct size in polar map was calculated as the percentage of lower threshold area in polar map from the total polar map area. The measured infarct size using different threshold methods was evaluated by comparison with reference infarct size. The mean difference between with polar map defect size by predefined thresholds (20%, 30%, and 40%) and reference infarct size were $7.04{\pm}3.44%$, $3.87{\pm}2.09%$ and $2.15{\pm}2.07%$, respectively. Otsu verse reference infarct size was $3.56{\pm}4.16%$. MGMM methods verse reference infarct size was $2.29{\pm}1.94%$. The predefined threshold (30%) showed the smallest mean difference with reference infarct size. However, MGMM was more accurate than predefined threshold in under 10% reference infarct size case (MGMM: 0.006%, predefined threshold: 0.59%). In this study, we was to evaluate myocardial infarct size in polar map using multiple Gaussian mixture model. MGMM method was provide adaptive threshold in each subject and will be a useful for automatic measurement of infarct size.

• Journal of radiological science and technology
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• v.24 no.2
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• pp.19-22
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• 2001

The purpose of this study is to evaluate time course of signal enhancement on Gadomer-17 enhance MRI, and to correlate the size of enhanced area with that of the infarct area on 2'3'5'-triphenyl tetrazolium chloride(TTC) histochemical examination for the assessment of myocardial viability in reperfused Myocardial Infarction in a cat model. Tan cats(average weight: 3.8 kg) which had undergone 90 minutes of occlusion of the LAD followed by 90 minutes of reperfusion underwent MR T2-weighted imaging, and T1-weighted imaging, enhanced T1-weighted imaging. We used 1.5T Magneton Vision MRI system(Siemens, Erlangen, Germany). Signal intensities were measured in the enhanced and non-enhanced areas of enhanced T1-weighted imaging. and TTC histochemical staining the size of the abnormal signal area on each image was compared with that of the infarct area. Maximum enhancement was detected during a $40{\sim}60$ minute period with an average enhancement of $168{\pm}9.9%$ of normal myocardium. TTC staining revealed that the size of the high signal area on T2-weighted images and of the enhanced area on enhanced T1-weighted images was greater than that of the infarct area($T2=48.1%{\pm}3.7$, enhanced $T1=47.2%{\pm}2.6$, TTC $staining=38.7%{\pm}3.1$ ; p<0.05). In reperfused Myocardial Infarction in a cat model, enhanced MR imaging delineates reversibly and irreversibly damaged myocardium, with a strong enhancement and a broad temporal window. We may therefore expect that enhanced MR image is useful for demonstrating myocardial injury.

• Journal of Cardiovascular Imaging
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• v.30 no.3
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• pp.169-180
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• 2022

BACKGROUND: We analyzed whether C-11 acetate positron emission tomography (PET) can be used for the evaluation of non-infarct-related artery (NIRA) in patients with ST-elevation myocardial infarction (STEMI) and multivessel disease. METHODS: We prospectively enrolled 31 patients with STEMI and at least one NIRA stenosis (diameter stenosis [DS] ≥ 50%). C-11 acetate PET was performed after successful revascularization for the infarct-related artery (IRA). Myocardial blood flow (MBF) and oxidative metabolism (k_mono) were measured and compared between NIRA vs. IRA, stenotic (DS ≥ 50%) vs. non-stenotic (DS < 50%) NIRAs, and NIRAs with significant stenosis (DS ≥ 70% or fractional flow reserve [FFR] ≤ 0.80) vs. those without (neither DS ≥ 70% nor FFR ≤ 0.80). The correlations between PET and angiographic parameters were also analyzed. RESULTS: MBF and k_mono were significantly higher in NIRAs than those in IRAs. Stenotic NIRAs showed significantly reduced stress MBF, myocardial flow reserve (MFR), relative flow reserve (RFR) (0.72 ± 0.12 vs. 0.82 ± 0.14; p = 0.001), and stress k_mono, as compared to those in non-stenotic NIRAs. NIRAs with significant stenosis had significantly lower stress MBF, MFR, and RFR (0.70 ± 0.10 vs. 0.80 ± 0.14; p = 0.001). RFR showed the best, but modest linear correlation with DS of NIRA stenosis (r = -0.429, p = 0.001). RFR > 0.81 could effectively exclude the presence of significant NIRA stenosis. CONCLUSIONS: C-11 acetate PET could be a feasible alternative noninvasive modality in patients with STEMI and multivessel disease, by excluding the presence of significant NIRA stenosis.

• Journal of Chest Surgery
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• v.46 no.6
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• pp.433-438
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• 2013

Background: Surgical repair of post-infarct ventricular septal defect (VSD) is considered one of the most challenging procedures having high surgical mortality. This study aimed to evaluate the outcomes of the surgical repair of post-infarct VSD. Methods: From May 1991 to July 2012, 34 patients (mean age, $67.1{\pm}7.9$ years) underwent surgical repair of post-infarct VSD. A retrospective review of clinical and surgical data was performed. Results: VSD repair involved the infarct exclusion technique using a patch in all patients. For coronary revascularization, 12 patients (35.3%) underwent concomitant coronary artery bypass graft, 3 patients (8.8%) underwent preoperative percutaneous coronary intervention, and 9 patients (26.5%) underwent both of these procedures. The early mortality rate was 20.6%. Six patients (17.6%) required reoperation due to residual shunt or newly developed VSD. During follow-up (median, 4.8 years; range, 0 to 18.4 years), late death occurred in nine patients. Overall, the 5-year and 10-year survival rates were $54.4%{\pm}8.8%$ and $44.3%{\pm}8.9%$, respectively. According to a Cox regression analysis, preoperative cardiogenic shock (p=0.069) and prolonged cardiopulmonary bypass time (p=0.008) were independent predictors of mortality. Conclusion: The early surgical outcome of post-infarct VSD was acceptable considering the high-risk nature of the disease. The long-term outcome, however, was still dismal, necessitating comprehensive optimal management through close follow-up.