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Background: Angiogenesis has increasingly been a target for imaging and treatment over the last decade. The integrin α v β 3 is highly expressed in cells during angiogenesis and are therefore a promising target for imaging. In this study, we aimed to investigate the PET tracer [ 68 Ga]Ga-RGD as a marker of angiogenesis following MI and its ability to predict cardiac functional parameters., Methods: First, the real-time interaction between [ 68 Ga]Ga-RGD and integrin α v β 3 was investigated using surface plasmon resonance (SPR). Second, an animal study was performed to investigate the [ 68 Ga]Ga-RGD uptake in the infarcted area after one and four weeks following MI in a rat model (MI = 68, sham surgery = 36). Finally, the specificity of the [ 68 Ga]Ga-RGD tracer was evaluated ex vivo using histology, autoradiography, gamma counting and flow cytometry., Results: SPR showed that [ 68 Ga]Ga-RGD has a high affinity for integrin α v β 3 , forming a strong and stable binding. PET/CT showed a significantly higher uptake of [ 68 Ga]Ga-RGD in the infarcted area compared to sham one week (p < 0.001) and four weeks (p < 0.001) after MI. The uptake of [ 68 Ga]Ga-RGD after one week correlated to end diastolic volume (r = 0.74, p < 0.001) and ejection fraction (r = - 0.71, p < 0.001) after four weeks., Conclusion: This study demonstrates that [ 68 Ga]Ga-RGD has a high affinity for integrin α v β 3 , which enables the evaluation of angiogenesis and remodeling. The [ 68 Ga]Ga-RGD uptake after one week indicates that [ 68 Ga]Ga-RGD may be used as an early predictor of cardiac functional parameters and possible development of heart failure after MI. These encouraging data supports the clinical translation and future use in MI patients., (© 2023. The Author(s).)

Background: Endogenous calcitonin gene-related peptide (CGRP) induces cardioprotective effects through coronary vasodilation. However, the systemic administration of CGRP induces peripheral vasodilation and positive chronotropic and inotropic effects. This study aims to examine the net effect on coronary perfusion of the systemically administered α-calcitonin gene-related peptide analogue, SAX, in rats during myocardial infarction., Methods: Forty Sprague-Dawley rats underwent myocardial infarction. Following left anterior descending artery occlusion, [ 99m Tc]Tc-sestamibi was administered to determine the myocardial perfusion before treatment. Twenty minutes, 24 and 48 h after [ 99m Tc]Tc-sestamibi injection, the rats were treated with either SAX or placebo. Final infarct size was determined three weeks later by [ 99m Tc]Tc-sestamibi SPECT/CT scan., Results: Thirty-one rats survived the surgery and 20 completed the follow-up SPECT/CT scan (SAX n = 12; Placebo n = 8). At baseline, there was no difference in size of perfusion defect between the groups (P = .88), but at follow-up the SAX group had improved myocardial recovery compared to the placebo group (P = .04), corresponding to a relative perfusion recovery of 55% in SAX-treated rats., Conclusion: The CGRP analogue, SAX, has a cardioprotective effect in this rat model of myocardial infarction, improving myocardial perfusion recovery after chronic occlusion of the coronary artery., (© 2021. The Author(s).)

Angiogenesis is involved in regeneration of cardiac tissue following acute myocardial infarction (MI), a disease often investigated in rat models. Therefore, the ability to thoroughly evaluate the angiogenic response following experimentally induced MI in rats, and distinguish it from inflammation, is desired. This would enable evaluation of the angiogenic potential of new therapeutics and improve knowledge on MI pathophysiology. Due to the complex response to MI involving multiple cell types and the limited selection of rat-specific antibodies, careful optimization is crucial to capture this complexity. Here, we present an 8-color flow cytometry-based multicolor panel that will enable quantification of the ongoing angiogenic response as well as characterize the cells involved. A detailed description of tissue preparation, immunostaining, and gating strategy is provided. © 2021 Wiley Periodicals LLC. Basic Protocol: Cardiac tissue preparation and staining to investigate the ongoing angiogenic response in rat cardiac tissue following myocardial infarction Support Protocol: Titration of all antibodies in the presented panel., (© 2021 Wiley Periodicals LLC.)

Background: Small-animal myocardial infarct models are frequently used in the assessment of new cardioprotective strategies. A validated quantification of perfusion using a non-cyclotron-dependent PET tracer would be of importance in monitoring response to therapy. We tested whether myocardial PET perfusion imaging is feasible with Rubidium-82 ( 82 Rb) in a small-animal scanner using a rat myocardial infarct model., Methods: 18 Sprague-Dawley rats underwent permanent coronary artery ligation (infarct group), and 11 rats underwent ischemia-reperfusion (reperfusion group) procedure. 82 Rb-PET and magnetic resonance imaging (MRI) were conducted before and after the intervention. Perfusion was compared to both left ventricle ejection fraction (LVEF) and infarct size assessed by MRI., Results: Follow-up global 82 Rb-uptake correlated significantly with infarct size (infarct group: r = -0.81, P < 0.001 and reperfusion group: r = -0.61, P = 0.04). Only 82 Rb-uptake in the infarct group correlated with LVEF. At follow-up, a higher segmental 82 Rb-uptake in the infarct group was associated with better wall motion (β = 0.034, CI [0.028;0.039], P < 0.001, R 2  = 0.30), and inversely associated with scar transmurality (β = -2.4 [-2.6; -2.2], P < 0.001, R 2  = 0.59). The associations were similar for the reperfusion group., Conclusion: 82 Rb-PET is feasible in small animal scanners despite the long positron range and enables fast and time-efficient myocardial perfusion imaging in rat models.

Background: Lectin complement pathway (LP) activation is an important mechanism in myocardial ischemia reperfusion injury (IRI). LP is activated via the recognition molecules mannose-binding lectin (MBL), ficolins-2 and-3 and is regulated by MBL/Ficolin-associated Protein-1 (MAP-1). Also, C-reactive protein (CRP) and ficolin-2 interact in vitro, but the role of the ficolins in IRI is unknown., Methods and Results: In 55 patients with ST segment elevation myocardial infarction, we investigated the association of LP components and CRP in plasma samples with left ventricular (LV) end systolic and diastolic volumes (ESV and EDV) and infarct size, assessed by cardiac magnetic resonance early at 1-3 days after primary percutaneous coronary intervention and at 6 months follow-up. Opposed to MBL, ficolin-3 and MAP-1, ficolin-2 levels were low at baseline. At baseline, ficolin-2>median was associated with ESV and EDV increases by 7.83 ml/m(2) (p=0.004) and 14.04 ml/m(2) (p<0.001). MBL and MAP-1 were not associated with LV dilatation, yet ficolin-2 and MBL worked synergistically and the combination of their levels>median was associated with ESV (11.21 ml/m(2); p=0.017) and EDV increases (14.72 ml/m(2); p=0.006). MAP-1median had the greatest LV dilatation (17.61 ml/m(2)). The ficolin-2 × CRP interaction variable was positively associated with infarct size and inversely associated with EDV change over 6 months (p=0.006). There was no interaction between CRP and the other LP molecules., Conclusion: The LP initiator molecule ficolin-2 and combinations of ficolin-2, MBL and MAP-1 are associated with LV dilatation after myocardial infarction. Interaction of ficolin-2 and CRP was associated with infarct size and LV remodeling, indicating a potential role for LP and LP-pentraxin cross-activation in IRI and LV remodeling., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Background: Granulocyte-colony-stimulating factor (G-CSF) has been investigated in trials aiming to promote recovery of myocardial function after myocardial infarction. Long-term safety-data have never been reported. A few studies indicated an increased risk of in-stent re-stenosis. We aimed to investigate clinical events 5 years after inclusion into a randomized trial of G-CSF versus placebo., Methods: Seventy-eight patients were randomized, from 2003-2005, to G-CSF or placebo after myocardial infarction. Four patients withdrew consent prior to study treatment and were excluded leaving 36 and 38 in the placebo- and G-CSF groups. Information about all hospital admittances of included patients until 2010 was extracted from a national register. The only censoring event was immigration. The events were combined into four prespecified endpoints: Time to (1) first hospital admittance (all cause), (2) first cardiovascular-related hospital admittance, (3) first major cardiovascular event, and (4) death., Results: One patient (1%) was lost to follow-up. Four patients (4%) died in the follow-up period, three in the G-CSF group and one in the placebo group (p = 0.4). Hazard ratio for all cause hospital admittance was 0.7 (95% CI 0.38-1.29). The incidence of both new myocardial infarction (p = 1.0) and revascularization procedures (p = 0.4) were similar in the two groups. Survival analyses showed no differences in the occurrence of any of the four prespecified composite endpoints between the two groups (p = 0.6; 0.5; 0.8; 0.3)., Conclusions: We found no indication of increased risk of adverse events up to 5 years after G-CSF treatment. These results support the continued investigation of G-CSF for cardiac therapy.

Background: Granulocyte-colony stimulating factor (G-CSF) therapy after ST-elevation myocardial infarction (STEMI) have not demonstrated impact on systolic recovery compared to placebo. However, recent studies suggest that timing of G-CSF therapy is crucial., Methods: Timing of G-CSF treatment was analyzed in the STEMMI MRI subpopulation including 54 patients with STEMI treated with primary percutaneous coronary intervention (PCI) <12 h after symptom onset. Patients were randomized to double blind treatment with G-CSF (10 microg/kg/day) or placebo. Treatment was initiated from 17 to 65 h (mean 30) after PCI. Left ventricular ejection fraction (LVEF) was evaluated with MRI., Results: Recovery of LVEF from baseline to 6 months was not associated with time from PCI to G-CSF. An identical improvement in LVEF was found in the placebo group and the G-CSF group (p=0.8). There was no correlation between time from PCI to G-CSF and maximum plasma concentration of CD34+ cells (r=-0.3, p=0.1). Similar results were found from data on recovery of the infarction size and change in the systolic wall thickening., Conclusions: In the time window from 17 to 65 h after STEMI treated with PCI, the timing of G-CSF treatment does not seem to affect the recovery of LVEF. It remains to be determined if very early, or very late G-CSF treatment might be effective., (Copyright (c) 2008 Elsevier Ireland Ltd. All rights reserved.)

Background: Plasma YKL-40 is increased early in patients with ST-elevation myocardial infarction (STEMI). It is not known whether plasma YKL-40 is related to infarct size and recovery of ventricular function after primary percutaneous coronary intervention (PCI) of STEMI and whether granulocyte colony-stimulating factor (G-CSF) therapy influence plasma YKL-40 concentration., Materials and Methods: A total of 72 patients (age: 56 +/- 9 years (mean +/- SD), 56 men and 16 women) with STEMI treated with PCI were included in a double-blind, randomized, placebo-controlled trial with subcutaneous G-CSF or placebo injections from day 1 to 7 after the STEMI. Plasma YKL-40, high-sensitivity C-reactive protein (hs-CRP) and CK-MB concentrations were measured at baseline and during the first month. Infarct size and left ventricular ejection fraction (LVEF) were measured by magnetic resonance imaging at baseline and after 6 months., Results: Baseline plasma YKL-40 was increased (median 92 microg/L) compared to healthy subjects (median 34 microg/L, p <0.001). In the placebo group hs-CRP and YKL-40 correlated at baseline (p = 0.04) and day 3 (p = 0.01), but not at day 7 and 30. Moreover, YKL-40 correlated negatively to LVEF recovery (p = 0.04) but not infarct size. G-CSF injections increased YKL-40 compared to placebo (p <0.001), but were not associated with infarct size or LVEF recovery., Conclusion: Plasma YKL-40 was significantly increased in STEMI patients at admission and G-CSF treatment caused a further increase in YKL-40. Plasma YKL-40 may be an indirect marker of LVEF recovery, independent of hs-CRP, and higher plasma YKL-40 indicates a lower recovery.

Background: Recombinant granulocyte-colony stimulating factor (G-CSF) mobilized pluripotent cells from the bone marrow are proposed to have a regenerative potential. Though, a report of excessive instent restenosis, in patients treated with G-CSF before percutaneous coronary intervention (PCI) warrants caution., Methods: Patients (n=59) enrolled in the STEMMI trial, a randomized and double blind study, comparing G-CSF and placebo after large ST-elevation myocardial infarctions, had an intracoronary ultrasound imaging at 6 months follow-up with a quantitative analysis of instent neointimal hyperplasia., Results: During G-CSF treatment leukocyte counts, and CD34+ and CD45-/CD34- cell fractions in peripheral blood increased markedly (p<0.0001 vs. placebo). At follow-up, there were no differences in intracoronary late lumen loss, expressed as neointima volume per mm of stent (1.6 mm(3)± 1.2 [G-CSF group] vs. 1.9 mm(3)± 1.3 [placebo group]; p=0.38), and in minimal instent lumen area (5.4 mm(2)± 2.4 vs. 5.3 mm(2)± 2.6, p=0.90). In the placebo group, plasma concentration of stromal cell-derived factor-1 (SDF-1) increased significantly after STEMI. This SDF-1 response was completely suppressed during G-CSF treatment. A rebound increase of SDF-1 was observed after withdrawal of G-CSF (p=0.001). Plasma concentration of SDF-1 at the time of stent implantation correlated positively to neointimal hyperplasia (p=0.025)., Conclusions: G-CSF treatment, initiated after PCI, does not lead to excessive instent neointimal hyperplasia or restenosis in patients with STEMI. The timing of G-CSF, in relation to the PCI, might be important, as G-CSF influences SDF-1., (Copyright © 2008 Elsevier Ireland Ltd. All rights reserved.)

This review of adjunctive therapy with subcutaneous granulocyte-colony stimulating factor (G-CSF) to patients with acute myocardial infarction (AMI) focus on the cardioprotective effects and potential mechanisms of G-CSF and discuss the therapeutic potential of G-CSF. All clinical trials published in peer-reviewed journals identified through PubMed are discussed. G-CSF treatment seems to be safe, and initial unblinded trials in patients with AMI were encouraging. However, larger double-blind placebo-controlled trials have not been able to demonstrate improved myocardial recovery after G-CSF treatment. Current controversies in interpretation of the results include 1) importance of direct cardiac effect of G-CSF vs indirect through bone marrow stem and progenitor cell mobilization, 2) importance of timing of G-CSF therapy, 3) importance of G-CSF dose, and 4) importance of cell types mobilized from the bone-marrow. Cell-based therapies to improve cardiac function remain promising and further experimental and clinical studies are warranted to determine the future role of G-CSF.

Objectives: The objective of this meta-analysis was to evaluate the effect of stem cell mobilization by granulocyte colony-stimulating factor (G-CSF) on myocardial regeneration on the basis of a synthesis of the data generated by randomized, controlled clinical trials of G-CSF after acute myocardial infarction (AMI)., Background: Experimental studies and early-phase clinical trials suggest that stem cell mobilization by G-CSF may have a positive impact on cardiac regeneration after AMI. The role of G-CSF in patients with AMI remains unclear considering the inconsistent results of several clinical trials., Methods: For our analysis, PubMed, the Cochrane Central Register of Controlled Trials, conference proceedings from major cardiology meetings, and Internet-based sources of information on clinical trials in cardiology from January 2003 to August 2007 served as sources. Two reviewers independently identified studies and abstracted data on sample size, baseline characteristics, and outcomes of interest. Eligible studies were randomized trials with stem cell mobilization by G-CSF after reperfused AMI that reported data regarding the change in left ventricular ejection fraction (LVEF) at follow-up., Results: Ten trials using stem cell mobilization by G-CSF, including 445 patients, met the inclusion criteria. Significant improvement in LVEF at follow-up was observed in both the G-CSF and placebo groups. Compared with placebo, stem cell mobilization by G-CSF did not enhance the improvement of LVEF at follow-up (mean difference 1.32% [95% confidence interval -1.52 to 4.16; p = 0.36]). Moreover, the mean difference of reduction of infarct size between the treatment and placebo groups was -0.15 (95% confidence interval -0.38 to 0.07, p = 0.17)., Conclusions: Cumulatively, available evidence does not support a beneficial effect of G-CSF in patients with AMI after reperfusion.

Background: Knowledge of the natural course after an ST-elevation myocardial infarction (STEMI) treated according to guidelines is limited because comprehensive serial magnetic resonance imaging (MRI) of systolic left ventricular function, edema, perfusion, and infarct size after STEMI has not been undertaken. The aim of this study was to evaluate effects of therapy for STEMI on left ventricular function and perfusion and to test the hypothesis that myocardial perfusion by MRI predicts recovery of left ventricular function., Methods: Cine MRI, edema, first-pass perfusion, and late enhancement imaging were performed in 58 patients at day 2 and at 1 and 6 months after successful primary percutaneous coronary stent intervention for STEMI., Results: Ejection fraction increased 6.3% during the first month (P < .001) and 1.9% from 1 to 6 months (P < .06), indicating a maximal recovery very early after the infarction. The systolic wall thickening in the infarct area almost doubled (P < .001), the perfusion of infarcted myocardium increased approximately 50% (P = .02), and perfusion improved in 72% of patients. Edema decreased with a mean of 2 segments (P < .001) during the first month and another 2.5 segments from 1 to 6 months (P < .001). Infarct size decreased to 1 month (P = .01) and was unchanged from 1 to 6 months (P = .5). Baseline perfusion did not predict improvement in ejection fraction (r = 0.2, P = .2) but did predict regional systolic function (P = .03)., Conclusions: Left ventricular function, perfusion, and infarct mass recovered substantially after STEMI, with the main part of the change within the first month. First-pass perfusion at rest appeared to predict regional ventricular recovery.

Background: Granulocyte-colony stimulating factor (G-CSF) after myocardial infarction does not affect systolic function when compared with placebo. In contrast, intracoronary infusion of bone marrow cells appears to improve ejection fraction. We aimed to evaluate the G-CSF mobilization of subsets of stem cells., Methods and Results: We included 78 patients (62 men; 56+/-8 years) with ST-elevation myocardial infarction treated with primary percutaneous intervention <12 hours after symptom onset. Patients were randomized to double-blind G-CSF (10 microg/kg/d) or placebo. Over 7 days, the myocardium was exposed to 25x10(9) G-CSF mobilized CD34+ cells, compared with 3x10(9) cells in placebo patients (P<0.001); and to 4.9x10(11) mesenchymal stem cells, compared with 2.0x10(11) in the placebo group (P<0.001). The fraction of CD34+ cells/leukocyte increased during G-CSF treatment (from 0.3+/-0.2 to 1.1+/-0.9 x10(-3), P<0.001 when compared with placebo), whereas the fraction of putative mesenchymal stem cells/leukocyte decreased (from 22+/-17 to 14+/-11 x10(-3), P=0.01 when compared with placebo). An inverse association between number of circulating mesenchymal stem cells and change in ejection fraction was found (regression coefficient -6.8, P=0.004), however none of the mesenchymal cell subtypes analyzed, were independent predictors of systolic recovery., Conclusions: The dissociated pattern for circulating CD34+ and mesenchymal stem cells could be attributable to reduced mesenchymal stem cell mobilization from the bone marrow by G-CSF, or increased homing of mesenchymal stem cells to the infarcted myocardium. The inverse association between circulating mesenchymal stem cells and systolic recovery may be of clinical importance and should be explored further.

Background: Acute treatment strategy and subsequently prognosis are influenced by the duration of ischemia in patients with ST-elevation acute myocardial infarction (AMI). However, timing of ischemia may be difficult to access by patient history (historical timing) alone. We hypothesized that an electrocardiographic acuteness score is better than historical timing for predicting myocardial salvage and prognosis in patients with anterior AMI treated with fibrinolysis or primary percutaneous coronary intervention., Methods: One hundred seventy-five patients with anterior infarct without electrocardiogram (ECG) confounding factors were included. The ECG method for estimating timing of AMI was calculated using core laboratory measurements from the initial 12-lead ECG. Historical timing was recorded as time from symptom onset to initiation of reperfusion therapy. Myocardial salvage was determined by ECG, using the Aldrich score to determine the initially predicted myocardial infarct size and the Selvester score to determine the final QRS-estimated myocardial infarct size., Results: The mean amount of myocardium salvage depended on ECG timing (43% [+/-38%] for "early" vs 1% [+/-56%] for "late"; P < .001), whereas myocardial salvage was independent of historical timing (P = .9). One-year mortality was predicted from ECG timing (P = .04)., Conclusions: The ECG method of timing was superior to historical timing in predicting myocardial salvage and prognosis after reperfusion therapy. This study suggests that ECG estimated duration of ischemia might provide a better and objective means to select acute reperfusion therapy rather than the subjective patient history, which could preclude proper reperfusion in some patients with salvageable myocardium.

Objective: To determine whether ischaemia grade (GI) on the presenting ECG and duration of symptoms can identify subgroups of patients who would derive more benefit than the general population of patients with ST segment elevation acute myocardium infarction (STEMI) from primary percutaneous coronary intervention (pPCI) over thrombolytic treatment (TT) in reducing mortality or reinfarction., Methods: 1319 DANAMI-2 (Danish trial in Acute Myocardial Infarction-2) patients were classified as having grade 2 ischaemia (GI2; ST segment elevation without terminal QRS distortion) or grade 3 ischaemia (GI3; ST segment elevation with terminal QRS distortion in > or = 2 adjacent leads), and were divided into early and late groups split by the median time (3 h) from symptom onset to treatment. Outcomes were 30-day mortality and reinfarction., Results: Mortality was significantly higher for GI3 than for GI2 (9.7% v 4.8%, p < 0.001) and doubled for patients presenting late (GI2: 6.0% v 3.3%, p = 0.01; GI3: 12.5% v 4.7%, p = 0.05). Overall mortality did not differ significantly between pPCI and TT; however, a 5.5% absolute mortality reduction was seen in GI3 treated early with pPCI (1.4% v 6.9%, p = 0.10). Reinfarction rate was particularly high among GI3 patients presenting late and treated with TT (12.2%). pPCI in such patients significantly reduced the rate of reinfarction (0%, p < 0.001). Logistic regression analysis showed that age (odds ratio (OR) 1.09, 95% confidence interval (CI) 1.06 to 1.12, p < 0.001), prior angina (OR 2.56, 95% CI 1.44 to 4.54, p = 0.001), heart rate (OR 1.03, 95% CI 1.01 to 1.04, p = 0.001) and GI3 (OR 1.91, 95% CI 1.06 to 3.44, p = 0.031) were independently associated with mortality, whereas the sum of ST segment elevation was not., Conclusions: GI3 is an independent predictor of mortality among patients with STEMI. Mortality increased significantly with symptom duration in both GI2 and GI3. pPCI may be especially beneficial for patients with GI3 presenting early, whereas patients with GI3 presenting late and treated with TT are at particular risk of reinfarction.

Objective: To investigate the spontaneous occurrence of circulating mesenchymal stem cells (MSC) and angiogenic factors in patients with ST elevation acute myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI)., Design: In 20 patients with STEMI, blood samples were obtained on days 1, 3, 7, 14, 21, and 28 after the acute PCI. Fifteen patients with a normal coronary angiography formed a control group. MSC (CD45-/CD34-), plasma stromal derived factor 1 (SDF-1), vascular endothelial growth factor A (VEGF-A), and fibroblast growth factor 2 (FGF-2) were measured by multiparametric flow cytometry and enzyme linked immunosorbent assay (ELISA)., Results: Circulating CD45-/CD34- cells were significantly decreased on day 7 compared with day 3. Cell counts normalised one month after the acute onset of STEMI. The changes were mainly seen in patients with a large infarction. Plasma SDF-1 increased significantly from day 3 to day 28, and VEGF-A and FGF-2 increased significantly from day 7 to day 28., Conclusions: Spontaneous sequential fluctuations in MSC and the increase in vascular growth factor concentrations after STEMI suggest that the optimal time for additional stem cell therapy is three weeks after a myocardial infarction to obtain the maximum effects by stimulating endogenous growth factors on the delivered stem cells.

Background: Phase 1 clinical trials of granulocyte-colony stimulating factor (G-CSF) treatment after myocardial infarction have indicated that G-CSF treatment is safe and may improve left ventricular function. This randomized, double-blind, placebo-controlled trial aimed to assess the efficacy of subcutaneous G-CSF injections on left ventricular function in patients with ST-elevation myocardial infarction., Methods and Results: Seventy-eight patients (62 men; average age, 56 years) with ST-elevation myocardial infarction were included after successful primary percutaneous coronary stent intervention <12 hours after symptom onset. Patients were randomized to double-blind treatment with G-CSF (10 microg/kg of body weight) or placebo for 6 days. The primary end point was change in systolic wall thickening from baseline to 6 months determined by cardiac magnetic resonance imaging (MRI). An independent core laboratory analyzed all MRI examinations. Systolic wall thickening improved 17% in the infarct area in the G-CSF group and 17% in the placebo group (P=1.0). Comparable results were found in infarct border and noninfarcted myocardium. Left ventricular ejection fraction improved similarly in the 2 groups measured by both MRI (8.5 versus 8.0; P=0.9) and echocardiography (5.7 versus 3.7; P=0.7). The risk of severe clinical adverse events was not increased by G-CSF. In addition, in-stent late lumen loss and target vessel revascularization rate in the follow-up period were similar in the 2 groups., Conclusions: Bone marrow stem cell mobilization with subcutaneous G-CSF is safe but did not lead to further improvement in ventricular function after acute myocardial infarction compared with the recovery observed in the placebo group.

Background: Because patients with acute left circumflex occlusion are typically characterized primarily on the standard 12-lead electrocardiogram (ECG) by ST depression, they do not qualify to receive reperfusion therapy. Documentation of a relationship between the quantities of acute ST change and final QRS estimated acute myocardial infarction (AMI) size could form the basis for clinical trials to determine the value of reperfusion therapy., Method: The Fragmin and Fast Revascularization during Instability in Coronary artery disease trial included 3214 patients with unstable coronary artery disease. Two percent of the patients (n = 69) had maximum ST-segment depression in leads V 1 through V 3 and were selected for this study. Initial ECG changes were compared to final myocardial infarction size, using the Selvester QRS score as the end point., Results: The quantity of initial ST-segment deviation correlated with the final AMI size (r = 0.43, P < .0005). The formula 3[0.22 (SigmaST downward arrow + SigmaST upward arrow) -0.02], where downward arrow indicates depression and upward arrow elevation, derived from measurements on the initial ECG, predicted the size of the AMI in percentage of the left ventricle as estimated on the final ECG. The study population had a large proportion of AMI (73%) indicated to be in or adjacent to the posterior left ventricular wall., Conclusion: The quantitative initial ST-segment deviation correlates linearly to the final AMI size in patients with maximum ST-segment depression in leads V 1 through V 3. The formula derived could be valuable for selecting patients who fail to meet strict ST-elevation AMI criteria for emergency intravenous or intracoronary reperfusion therapy.

The Anderson-Wilkins (AW) electrocardiographic (ECG) acuteness score complements time from pain onset in prognostic stratification of patients with acute myocardial infarction (AMI). However, for the AW acuteness score to be of practical use in the acute situation, it must be an integral component of a commercial automated ECG analysis program. The objective of this study was to determine the concordance between human and computer measurements and calculation of the AW acuteness score. The mean difference in AW acuteness score was 0.11 +/- 0.66 for anterior and -0.07 +/- 1.24 for inferior AMI. Ninety-nine percent of the differences were found to be 1.0 or less for the anterior AMI group, and 91.7% were 1.0 or less in the inferior AMI group. The differences were primarily caused by minor disagreements in measurements. In conclusion, the AW acuteness score established using manual ECG waveform measurements can be implemented into commercial automated ECG analysis programs to achieve practical use in clinical decision support for patients with AMI.