Novel injectable alginate scaffold attenuates progressive infarct expansion and preserves left ventricular systolic and diastolic functions late after myocardial infarction

2006 ◽  
Vol 7 (2) ◽  
pp. 98
Author(s):  
N. Landa ◽  
M.S. Feinberg ◽  
R. Holbova ◽  
L. Miller ◽  
S. Cohen ◽  
...  
2012 ◽  
Vol 35 (4) ◽  
pp. 229 ◽  
Author(s):  
Fatih Poyraz ◽  
Murat Turfan ◽  
Sinan A. Kocaman ◽  
Huseyin U. Yazici ◽  
Nihat Sen ◽  
...  

Purpose: The purpose of this study was to evaluate whether a association exits among overweight and obesity and left ventricular systolic and diastolic functions in patients admitted with first ST-elevation myocardial infarction (STEMI). Methods: The present study was performed on 451 consecutive patients diagnosed with first STEMI (376 men, 75 women; mean age 56.1±10.8 years). The patients were classified into three groups based on their body mass index (BMI) as normal weight (BMI < 25 kg/m2), overweight (BMI: 25-29.9 kg/m2) and obese (BMI > 30 kg/m2). Echocardiographic features were evaluated and compared among the three groups. Results: Mitral annulus E velocities were higher in obese individuals than normal weight group (p < 0.01). In contrast, mitral A velocities were lower (p =0.03); consequently, E\A and E'\A' ratios were lower (both p =0.01) in the obese group with respect to normal weight group. When the correction of entire variations existing among the groups were performed using multivariate linear regressions analyses, it turned out that BMI was independently associated with E/A (β= -0.19, p =0.044) and with E'/A' (β= -0.016, p=0.021). Ejection fraction, wall motion score index and myocardial S velocities were comparable among the study groups (p > 0.05). Conclusion: These results suggest that while obesity has no adverse effect on the left ventricular systolic function, it has unfavorable consequences on the left ventricular diastolic function in the patients with first STEMI. In contrast, no unfavorable effects of overweight on the left ventricular systolic and diastolic function were detected.


1994 ◽  
Vol 127 (3) ◽  
pp. 499-509 ◽  
Author(s):  
Giorgio Golia ◽  
Paolo Marino ◽  
Francesco Rametta ◽  
Giorgio Paolo Nidasio ◽  
Maria Antonia Prioli ◽  
...  

Author(s):  
Pei Zhang ◽  
Tieluo Li ◽  
Katrina Williams ◽  
Shuyin Li ◽  
Xufeng Wei ◽  
...  

In the United States, over one million patients sustain left ventricular (LV) injury after myocardial infarction (MI). LV remodeling is an adaptive process of hypertrophy that includes infarct expansion, reduced contractility and LV dilation. Progressive enlargement of non-ischemic, hypocontractile myocardium in the adjacent zone (AZ) following the transmural MI has been identified clinically, which contributes to the development post-MI cardiomyopathy in patients. Till now, how the early regional biomechanical and cellular changes, particularly in the AZ, relate to LV remodeling process remains incompletely understood. This study aims to investigate the temporal and/or spatial variations of strain/stress and myocyte size in an ovine model with various MI sizes.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Yasuyuki Fujita ◽  
Makoto Kinoshita ◽  
Hiroshi Akimaru ◽  
Erika Akimaru ◽  
Miki Komatsu ◽  
...  

Background: A phase I clinical trial revealed the safety and potential efficacy of intracoronary (i.c.) infusion of bone marrow (BM) CD34+ cells in patients with acute myocardial infarction (AMI). The final results of the “PreSERVE AMI” randomized phase II trial will be obtained this year. Despite such clinical development, CD34+ cell therapy for AMI has been preclinically investigated in the rat and mouse models, but not large animals. Methods: AMI was induced by 60 min-balloon inflation and reperfusion in the left anterior descending artery of the farm swine. One week after AMI, swine were randomly allocated to receive i.c. infusion of 2х105/kg GCSF-mobilized human CD34+ cells (cell group, n=8) or saline (control group, n=7). Immunosuppression was maintained by intramuscular injection of cyclosporine daily from week 1 to 5. Magnetic resonance imaging was performed to assess cardiac function and infarct size at week 1 and 5. All swine were sacrificed at week 5. Chemical staining for isolectin B4 was performed to detect capillaries in the cardiac tissue. Results: Left ventricular ejection fraction (LVEF) significantly increased in cell group (42.9±5.2 at week 1 to 48.5±4.1% at week 5, p<0.05) but not control group (47.6±2.4 to 44.8±3.5%, p=NS). LV end-systolic volume (LVESV) decreased in cell group (38.3±4.9 to 31.4±5.3 ml, p<0.01) but not control group (35.4±5.4 to 37.7±5.4 ml, p=NS). Regional wall thickening (RWT) in the border zone increased in cell group (30.8±14.9 to 45.5±10.4%, p<0.01) but not control group (37.2±16.4 to 26.4±9.3%). Infarct size by delayed enhancement increased in control group (16.8±7.5 to 22.35±6.4% of LV mass, p<0.05) but not cell group (20.5±10.2 to 20.87±8.0%). Changes in LVEF, LVESV and RWT between week 1 and 5 were better preserved in cell group than control group (p<0.05, 0.05 and 0.01, respectively). Histological capillary density in border zone was greater in cell group than control group (1698.0±474.2 vs 998.6±269.6/mm2, p<0.01). Conclusions: Human CD34+ cell therapy may preserve global and regional LV function and prevent infarct expansion through enhancing neocapillary formation in swine with AMI. The favorable outcomes would support the further clinical development of the cell-based therapy in patients with AMI.


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