Background Despite rapid clinical translation and widespread enthusiasm, the therapeutic benefits of adult bone marrow cell (BMC) transplantation in patients with ischemic heart disease (IHD) continue to remain controversial. A synthesis of the available data is critical to appreciate and underscore the true impact of this promising approach. Methods and Results A total of 50 studies (enrolling 2,625 patients) identified by database searches through January 2012 were included. Weighted Mean Differences for changes in left ventricular (LV) ejection fraction (LVEF), infarct size, LV end-systolic volume (LVESV), and LV end-diastolic volume (LVEDV) were estimated using random effects meta-analysis. Compared with controls, BMC-treated patients exhibited greater LVEF (3.96%, 95% confidence interval (CI): 2.90, 5.02; P<0.00001), and smaller infarct size (–4.03%, CI: –5.47, –2.59; P<0.00001), LVESV (–8.91 ml, CI: –11.57, –6.25; P<0.00001), and LVEDV (–5.23 ml, CI: – 7.60, –2.86; P<0.0001). These benefits were noted irrespective of the study design (RCT vs. Cohort study) and the type of IHD (acute myocardial infarction vs. chronic IHD), and persisted during long-term follow-up. Importantly, the all-cause mortality, cardiac mortality, and the incidence of recurrent MI and stent thrombosis were significantly lower in BMC-treated patients compared with controls. Conclusions Transplantation of adult BMCs improves LV function, infarct size, and remodeling in patients with IHD compared with standard therapy, and these benefits persist during long-term follow-up. BMC transplantation also reduces the incidence of death, recurrent MI, and stent thrombosis in patients with IHD.

Osteoclast-like giant cells (OLGCs) are multinucleated cells of histiocytic lineage and have been identified in a wide array of neoplasms. In the uterus, they have most frequently been reported in association with leiomyosarcomas. This article describes a case of an osteoclast-like giant cell-rich uterine tumor that was essentially indistinguishable at the morphologic and immunophenotypic levels, from typical giant cell tumor of bone. This is the first example of such a case that has been reported in the uterus to the authors' knowledge.

We thank Dr Delewi and colleagues for a careful review of our report 1 and thoughtful comments. The authors point out that our meta-analysis of 50 trials did not include 3 large trials (REGENT [Myocardial Regeneration by Intracoronary Infusion of Selected Population of Stem Cells in Acute Myocardial Infarction], BONAMI [Bone Marrow in Acute Myocardial Infarction], and HEBE).2-4 As mentioned under "Study Selection," our meta-analysis included trials that reported data as mean and standard deviation. The REGENT trial 2 reported data with median values and therefore could not be included. As a preliminary screening step, we reviewed the titles of all reports retrieved through a stepwise search strategy, and the title of the HEBE trial stated that mononuclear cells were derived from bone marrow or peripheral blood. Because it is a standard practice to mobilize bone marrow cells prior to harvest from peripheral blood, we assumed mobilization with cytokine. After reviewing the full article, it appears that Hirsch et al did not mobilize bone marrow cells and reported results from bone marrow group and peripheral blood group separately.3 In the report by Herbots et al, 4 we were unable to definitively ascertain whether magnetic resonance imaging data were from the same patient population as in the earlier report from this group. Finally, our search strategy failed to identify the BONAMI trial. 5In light of the above, we analyzed data for all primary end points de novo after including data from BONAMI and HEBE and excluding data from Herbots et al. 4 In this new analysis (51 trials, 2787 patients), compared with control subjects, bone marrow cell-treated patients exhibited greater left ventricular ejection fraction (3.87%; 95% confidence interval, 2.81%-4.93%; P<0.00001) and smaller infarct size (−3.42%; confidence interval, −4.74% to −2.10%; P<0.00001), left ventricular end-systolic volume (−8.34 mL; confidence interval, −10.92 to −5.76 mL; P<0.00001), and left ventricular end-diastolic volume (−4.57 mL; confidence interval, −6.77 to −2.37 mL; P<0.00001). Importantly, these results are very similar to those reported in our original paper and uphold our original major conclusions. 1As for the subgroup analysis, we do agree that cell therapy mechanisms are likely different in acute versus chronic ischemic heart disease, but we also recognize that the difference in myocardial pathology is not the only difference among these studies. Since subgroup analysis is limited by the number of trials (and patients) in each subgroup, we chose to include all eligible studies when assessing the impact of one specific factor (for example, timing) despite the presence of other differences (pathology, cell number, ejection fraction, and such) among included studies. This inherent limitation with meta-analysis at present can be circumvented only with data from a much larger number of trials and patients in the future. DisclosuresNone. Vinodh

BACKGROUND New echocardiographic phenotypes of heart failure (HF) are focused on myocardial systolic involvement of the left ventricle (LV), either endocardial and/or transmural. PURPOSE. To study the pattern of myocardial involvement in patients (p) with HF with preserved left ventricular ejection fraction (pLVEF) and cardiac amyloidosis (CA). METHODS. Comparative study of 16 p with CA and HF with pLVEF, considering as cut point LVEF &gt; 50%, in NYHA class ≥ II / IV, and a control group of 16 healthy people. Longitudinal Strain (LS) and Circumferential Strain (CS) were calculated using 2D speckle-tracking echocardiography, along with Mitral Annulus Plane Systolic Excursion (MAPSE) and Base-Apex distance (B-A). Also, the following indexes were calculated: Twist (apical rotation + basal rotation, º); Classic Torsion (TorC): (twist/B-A, º/cm); Torsion Index (Tor.I): (twist/MAPSE, º/cm) and Deformation Index (Def.I): (twist/LS, º). We suggest the introduction of these dynamic torsion indexes as Tor.I and Def.I that include twist per unit of longitudinal systolic shortening of the LV instead of using TorC which is the normalisation of twist to the end-diastolic longitudinal diameter of the LV. RESULTS There were no differences of age between the groups (68.2 ± 11.5 vs 63.7 ± 2.8 years, p = 0.14). Global values of LS and CS were lower in p with CA indicating endocardial and transmural deterioration during systole, while TorC and Twist of the LV remained conserved in p with CA. However, there is an increase of dynamic torsion parameters such as Tor.I and Def.I that show an increased Twist per unit of longitudinal shortening of the LV in the CA group (Table). CONCLUSIONS In p with CA and HF with pLVEF, the impairment of LS and CS indicates endocardial and transmural systolic dysfunction. In these conditions, LVEF would be preserved at the expense of a greater dynamic torsion of the LV. Table LS (%) CS (%) Twist (º) TorC (º/cm) Tor.I (º/cm) Def.I (º/%) CA pLVEF (n = 16) -11.7 ± 4.2 17.2 ± 4.8 19.8 ± 8.3 2.5 ± 1.1 27.7 ± 13.5 -1.8 ± 0.9 Control Group (n = 15) -20.6 ± 2.5 22.7 ± 4.9 21.7 ± 6.1 2.7 ± 0.8 16.4 ± 4.7 -1.0 ± 0.3 p &lt; 0.001 &lt; 0.01 0.46 0.46 &lt; 0.01 &lt; 0.01 Dynamic Torsion Indexes and Classic Torion Parameters in pLVEF CA patients vs Control group.