Key result
Pericardial adipose flap transposition increases LVEF ~19% versus controls in a swine acute MI model.
Why the study?
Coronary artery occlusion leads to ventricular remodelling, heart failure, and cardiogenic shock, and novel strategies are needed to treat these complications.
Does transposition of a pericardial-derived vascular adipose flap improve LV function and limit myocardial remodeling in a swine model of acute myocardial infarction?
Does transposition of a pericardial-derived vascular adipose flap improve LV function and limit myocardial remodeling in a swine model of acute myocardial infarction?
Transposition of a vascularized pericardial fat flap over an acute myocardial infarct improves LV function and reduces adverse remodeling in a swine model.
No immediate clinical implications; leaves open translation of pericardial adipose flaps to human post-MI remodeling.
AIMS: Coronary artery occlusion is associated with the risk of ventricular remodelling, heart failure, and cardiogenic shock. Novel strategies are sought to treat these ominous complications. We examined the effect of a pericardial-derived fat flap secured over an acute infarct caused by coronary occlusion. METHODS AND RESULTS: A novel intervention consisting of the pericardial isolation of a vascularized adipose flap and its transposition fully covering acute infarcted myocardium was developed in the swine model of coronary artery ligation (n= 52). Left ventricular (LV) ejection fraction and LV end-diastolic and end-systolic volumes were assessed using magnetic resonance imaging (MRI). Infarct size and gene expression analysis were performed on Day 6 and 1 month. Histological changes, collagen volume fraction (CVF), and vascular density were also evaluated on postmortem sections. One month after the intervention, a 18.8% increase in LV ejection fraction (P= 0.007), and significant reductions in LV end-systolic (P= 0.009) and LV end-diastolic volumes (P= 0.03) were found in treated animals compared with the control-MI group. At Day 6, histopathology confirmed a significant infarct size reduction (P= 0.018), the presence of vascular connections at the flap-myocardium interface, and less apoptosis in the infarct border zone compared with control animals (P< 0.001). Up-regulation of genes involved in cell cycle progression, cellular growth and proliferation, and angiogenesis were identified within the flap. CONCLUSIONS: Our results indicate that a vascular fat flap exerts beneficial effects on LV function and limits myocardial remodelling. Future studies must confirm whether these findings provide an alternative therapeutic approach for myocardial salvage after infarction.
No takes yet. Share an insight, caveat, or question.
Gálvez‐Montón et al. (2011) studied Acute infarct caused by coronary occlusion (n=52). Pericardial-derived vascular adipose flap transposition vs. Control-MI group was evaluated on Left ventricular (LV) ejection fraction (18.8% increase, p=0.007). Transposition of a pericardial-derived vascular adipose flap over acute infarcted myocardium in a swine model increased LV ejection fraction by 18.8% (P=0.007) at 1 month compared with controls.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: