3 research outputs found

    Impact of beating heart left atrial ablation on left-sided heart mechanics

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    ObjectiveThe cut-and-sew Cox–Maze procedure is the gold standard for surgical treatment of atrial fibrillation, but it is associated with long-term impairment of left atrial mechanical function. We developed a bipolar, irrigated radiofrequency ablation device. We hypothesized that beating heart radiofrequency left atrial ablation would result in minimal acute changes in left atrial hemodynamics.MethodsSix healthy subjects were studied. Combination pressure-conductance catheters were inserted into the left atrium and ventricle. With the use of the device, atrial ablation was performed on the beating heart without cardiopulmonary bypass, including electrical isolation of the posterior left atrium and atrial appendage myocardium. Simultaneous left-sided heart pressure–volume and intracardiac echocardiography data were acquired before ablation, after left atrial appendage ablation alone, and after all ablation (with and without appendage occlusion). The derived indices of left-sided heart mechanical function were examined.ResultsRelative to baseline, no significant diminishment in pressure–volume or intracardiac echocardiography-derived indices of global left-sided heart mechanical function were observed after ablation, with or without appendage occlusion. Mitral valve morphology and function were not significantly altered. A significant diminishment of atrial appendage systolic flow was noted after appendage ablation in association with spontaneous echocardiographic contrast in this region.ConclusionsIn this model, ablation does not seem to compromise global left-sided heart mechanical function. However, these findings mask regional diminishment in atrial appendage systolic function. This observation demonstrates that electrical isolation of the appendage should be accompanied by its occlusion or excision. Appendage occlusion after ablation does not seem to compromise left-sided heart mechanical function

    Autologous Biological Glue and Aprotinin Prevent Ischemia in Latissimus Dorsi Muscle after Mobilization

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    The hemodynamic results of cardiomyoplasty, a promising form of surgical treatment for end-stage heart failure, do not support the subjective improvements seen clinically. We hypothesized that this disparity might be due to ischemia-reperfusion injury to the latissimus dorsi muscle (LDM) after mobilization. Having tested autologous biological glue (ABG) as a protective layer around traumatized muscle, as a means for facilitating revascularization, and as a drug depot to reduce local ischemia-reperfusion lesions, we wanted to determine if this protective and revascularization effect could be enhanced by adding aprotinin, a natural inhibitor of serine proteinases with the potential for preventing proteolytic degradation. To test for muscle damage and angiogenesis, we created pockets out of ischemic and nonischemic LDM. The control group had pockets without additives; the second group had pockets with ABG only; and the third had pockets with ABG and aprotinin. Light microscopy revealed that pockets treated with ABG, either alone or with aprotinin, had less leukocyte margination, fibrosis, calcified necrosis, and fibrous degeneration than in controls. In control pockets, after 56 days, capillaries occupied 4.1 ± 0.3 % of the area in nonischemic LDM and 3.6 ± 0.7 % in ischemic LDM (p> 0.05). In pockets treated with ABG only, capillaries occupied 5.5 ± 0.2% (p < 0.05) of the area in ischemic LDM; in pockets treated with ABG and aprotinin, 8.5 ± 1.1% (p < 0.05) area was occupied with capillaries. This data confirmed our hypothesis that aprotinin added to ABG prevents ischemia-reperfusion lesions after muscle mobilization, and enhances capillary ingrowth in both the ischemic muscle and the interlayer between ischemic and nonischemic muscle. Key words: cardiomyoplasty, LDM ischemia, autologous biological glue, aprotinin
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