scholarly journals Validity of Resting Strain/strain Rate in Prediction of Myocardial Viability

2021 ◽  
Author(s):  
Amr Hanafy ◽  
Soliman Ghareb Ibrahim ◽  
Hossam Eldein Mohamed Mohamed Mansour ◽  
Aml Mohamed Soliman ◽  
Mohamed Kamal Salama
Keyword(s):  
Magnetic Resonance Imaging ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Magnetic Resonance ◽  
Magnetic Resonance ◽  
Strain Rate ◽  
Cardiac Magnetic Resonance Imaging ◽  
Myocardial Viability ◽  
Longitudinal Strain ◽  
Resonance Imaging

Abstract PurposeTo evaluate the validity of the resting strain/strain rate measurements in predicting myocardial viability taking delayed enhancement cardiac magnetic resonance imaging as the gold standard. Methods: A cohort of 60 patients at three months followed up after acute myocardial infarction were recruited for this study. Resting echocardiography with offline analysis of deformation indices and gadolinium contrast enhanced cardiac magnetic resonance imaging were applied for all patients. ResultsFor the final assessment, 268 segments with significant resting wall motion abnormalities were presented. Resting longitudinal strain was significantly (p<0.05) higher in viable, compared with non-viable segments in all the studied individual myocardial segments (apical inferior, mid antro-lateral, mid-inferolateral, mid infero-septum, and all other segments). Likewise, resting longitudinal strain rate was significantly (p<0.05) higher in viable, compared with non-viable segments in almost all studied individual myocardial segments apart from apical inferior, mid inferolateral and basal antro-septum (p=0.245, p=0.098, p=0.097 respectively). ConclusionResting Strain and Resting Strain rate could be used as accurate predictors of myocardia viability following acute myocardial infarction.

Small Endogeneous Peptide Mitigates Myocardial Remodeling in a Mouse Model of Cardioselective Galectin-3 Overexpression

2021 ◽  
Author(s):  
Swati D. Sonkawade ◽  
Saraswati Pokharel ◽  
Badri Karthikeyan ◽  
Minhyung Kim ◽  
Shirley Xu ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Cardiac Magnetic Resonance ◽  
Magnetic Resonance ◽  
Cardiac Magnetic Resonance Imaging ◽  
Cardiac Dysfunction ◽  
Resonance Imaging ◽  
Galectin 3

Background: Myocardial Gal3 (galectin-3) expression is associated with cardiac inflammation and fibrosis. Increased Gal3 portends susceptibility to heart failure and death. There are no data reporting the causative role of Gal3 to mediate cardiac fibro-inflammatory response and heart failure. Methods: We developed a cardioselective Gal3 gain-of-function mouse ( Gal3+/+ ) using α-myosin heavy chain promotor. We confirmed Gal3-transgene expression with real-time polymerase chain reaction and quantified cardiac/circulating Gal3 with Western blot and immunoassays. We used echocardiogram and cardiac magnetic resonance imaging to measure cardiac volumes, function, and myocardial velocities. Ex vivo, we studied myocardial inflammation/fibrosis and downstream TGF (transforming growth factor) β1-mRNA expression. We examined the effects of acute myocardial ischemia in presence of excess Gal3 by inducing acute myocardial infarction in mice. Two subsets of mice including mice treated with N-acetyl-seryl-aspartyl-lysyl-proline (a Gal3-inhibitor) and mice with genetic Gal3 loss-of-function ( Gal3 −/−) were studied for comparative analysis of Gal3 function. Results: Gal3+/+ mice had increased cardiac/circulating Gal3. Gal3+/+ mice showed excess pericardial fat pad, dilated ventricles and cardiac dysfunction, which was partly normalized by N-acetyl-seryl-aspartyl-lysyl-proline. Cardiac magnetic resonance imaging showed reduced myocardial contractile velocities in Gal3+/+ . The majority of Gal3+/+ mice did not survive acute myocardial infarction, and the survivors had profound cardiac dysfunction. Myocardial histology of Gal3+/+ mice showed macrophage/mast-cell infiltration, fibrosis and higher TGFβ1-mRNA expression, which were mitigated by both Gal3 gene deletion and N-acetyl-seryl-aspartyl-lysyl-proline administration. Conclusions: Our study shows that cardioselective Gal3 overexpression leads to multiple cardiac phenotypic defects including ventricular dilation and cardiac dysfunction. Pharmacological Gal3 inhibition conferred protective effects with reduction of inflammation and fibrosis. Our study highlights the importance of translational studies to counteract Gal3 function and prevent cardiac dysfunction.

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