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Abstract Background There is increasing interest in performing left atrial appendage (LAA) occlusion at the time of atrial fibrillation (AF) ablation procedures. However, to date there has been no description of the acute changes to the LAA immediately following pulmonary vein (PV) isolation and additional left atrium (LA) substrate modification. This study assessed changes in the size and tissue characteristics of the LAA ostium in patients undergoing PV isolation. Methods This series included 8 patients who underwent cardiovascular magnetic resonance evaluation of the LA with delayed enhancement magnetic resonance imaging and contrast enhanced 3-D magnetic resonance angiography pre-, within 48 h of, and 3 months post ablation. Two independent cardiac radiologists evaluated the ostial LAA diameters and area at each time point in addition to the presence of gadolinium enhancement. Results Compared to pre-ablation values, the respective median differences in oblique diameters and LAA area were +1.8 mm, +1.7 mm, and +0.6 cm2 immediately post ablation (all NS) and −2.7 mm, −2.3 mm, and −0.5 cm2 at 3 months (all NS). No delayed enhancement was detected in the LAA post ablation. Conclusion No significant change to LAA diameter, area, or tissue characteristics was noted after PV isolation. While these findings suggest the safety and feasibility of concomitant PV isolation and LAA device occlusion, the variability in the degree and direction of change of the LAA measurements highlights the need for further study.

The specific mechanisms by which diabetes may affect the myocardial tissue response to ischemia are unclear. Our objective was to prospectively quantify the degree of myocardial edema in diabetics versus nondiabetics with ST elevation myocardial infarction using cardiac magnetic resonance. Fifty-two patients (16 diabetics and 36 nondiabetics) were enrolled after primary percutaneous coronary intervention and underwent cardiac magnetic resonance on a 1.5-T scanner at 48 hours and 6 months. Myocardial edema was quantified using a T2 mapping technique, and infarct size and microvascular obstruction size were assessed by way of a contrast-enhanced T1-weighted inversion recovery gradient-echo sequence. The infarct segment T2 was elevated in diabetics compared with nondiabetics (59.0 ± 8.0 vs 50.8 ± 3.1 ms, p <0.001) at 48 hours. Multivariate analysis demonstrated that diabetes (p <0.001) and symptom-to-balloon time (p = 0.04) were independent predictors of the degree of acute myocardial edema. Infarct size was nonsignificantly higher in the diabetic group at 48 hours (26.9 ± 9.4% vs 20.1 ± 10.1% of myocardium, p = 0.07) and 6 months (17.1 ± 6.3% vs 13.4 ± 6.1% of myocardium, p = 0.09). Microvascular obstruction size was equivalent in both groups, and there was a trend toward lower myocardial salvage index in diabetics (34.2 ± 11.8 vs 49.6 ± 13.4, p = 0.08). In conclusion, diabetes is associated with increased myocardial edema in the acute phase after primary percutaneous coronary intervention. Our results offer insight into the complex processes that characterize myocardial tissue response to injury in diabetic patients.

Ischaemia reperfusion injury is a key cause of mortality and graft loss after liver transplantation. After tissue injury, monocytes are rapidly mobilised and recruited to injured tissue by monocyte chemoattractant protein-1 (MCP-1). Elevated MCP-1 concentrations correlate with poorer outcomes in patients after haemorrhagic stroke but have not been evaluated as a prognostic marker in clinical liver transplantation. We aimed to assess the role of inflammatory monocytes and MCP-1 in ischaemia reperfusion injury Adult patients undergoing liver transplantation at the Royal Free Hospital, London, UK, were recruited. Liver biopsy samples were collected preimplantation and 2 h after reperfusion from five patients. Intrahepatic mononuclear cells were extracted for immediate analysis by flow cytometery. Plasma MCP-1 concentrations from 33 patients were measured preoperatively by ELISA, 2 h and 24 h after reperfusion, and correlated with graft function by measurement of day 3 aspartate aminotransferase (AST) and early allograft dysfunction (EAD) score. Flow cytometric analysis demonstrated an increase in mean classical monocytes after reperfusion compared with preimplantation (4·18% of total live cells [SD 2·61] vs 0·61 [0·38], p=0·018). In three of the five recipients we distinguished cells of donor versus recipient origin by HLA-A allele expression to demonstrate that 88% (6·24) of the classical monocytes were recipient derived in the postreperfusion biopsy sample. Median MCP-1 concentrations were significantly raised after reperfusion (385·61 pg/mL [IQR 244·75–715·20] vs 71·2 [55·61–113·99], p<0·0001) and had reduced to 740·61 (38·46–133·71) within 24 h. Patients with EAD (n=17) had significantly higher MCP-1 concentrations at 24 h than those without EAD (74·82 [66·69–219·93] vs 47·44 [29·53–77·73], p=0·037). MCP-1 concentrations at 24 h correlated with day 3 AST concentrations (p=0·002). Our results show that classical monocytes are rapidly recruited to the liver after ischaemia reperfusion injury, and that high MCP-1 concentrations at 24 h are associated with poorer graft function. Therefore, MCP-1 blockade presents an attractive strategy to reduce graft ischaemia reperfusion injury. None.