Recurrence of left ventricular (LV) remodeling after surgical ventricular reconstruction (SVR) for ischemic cardiomyopathy has been reported to be partially attributed to autophagy. We aimed to examine the effects of trehalose, an autophagy inducer, on the recurrence of LV remodeling after SVR. After SVR in rats with ICM, trehalose was orally administered. The changes in LV end-diastolic dimension (LVEDD) and fractional shortening (FS) were evaluated. The activation of myocardial autophagy was also estimated by autophagy markers: microtubule-associated light chain 3 Ⅱ (LC3-Ⅱ) and p62; the former usually increases and the latter decreases if autophagy is activated.Significant LV reverse remodeling was observed early after SVR. On the other hand, the 28th postoperative day SVR + trehalose was associated with smaller LVEDD and better FS than SVR alone (LVEDD, P = 0.043; FS, P < 0.01). LC3-Ⅱ increased comparably in both groups, while p62 was significantly lower in the SVR + trehalose group than in the SVR alone group (P < 0.01). In conclusion, trehalose attenuated the recurrence of LV remodeling and changed autophagy markers after SVR in rats with ICM. Trehalose may be a candidate for adjuvant therapy to retain the effects of SVR.
We describe the surgical management of a 58-year-old man with inflammatory abdominal aortic aneurysm (IAAA) following treatment with preoperative steroids. The patient was transferred to our institution for abdominal pain and fever. Contrast-enhanced computed tomography showed juxtarenal abdominal aortic aneurysm surrounded by dense perianeurysmal fibrous tissue. Under a diagnosis of IAAA, steroid therapy with prednisolone was initiated to control the perianeurysmal inflammation. It continued for 3 weeks with a decreasing dose schedule, with remarkable decrease in the soft tissue mass. The patient underwent elective surgery 21 days after commencing steroid therapy. During surgery, adjacent organs were adherent to the aneurysmal wall, but fibrotic change to the retroperitoneum was very limited. He recovered uneventfully, and was discharged on postoperative Day 10. Therefore, it can be concluded that preoperative steroid therapy could minimize the operative risk for IAAAs, and improve surgical outcome.
Background:The change in myocardial protein degradation systems after ventricular unloading has been unknown. We aimed to evaluate the anti-hypertrophic protein adenosine monophosphate-activated protein kinase (AMPK) and two major protein degradation systems (ubiquitin proteasome system and autophagy) in a model of surgical ventricular reconstruction (SVR) in rats with ischemic cardiomyopathy.
Methods and Results:Rats were randomized into the following groups: sham/sham (control group), myocardial infarction (MI)/sham (sham group) and MI/SVR (SVR group), with an interval of 4 weeks. Two (early, n=5 for each) and 28 days (late, n=5 for each) after SVR, ventricular size, and wall stress were assessed. Myocyte area, protein expression of AMPKα and autophagy markers, and gene expression of ubiquitin ligases (Atrogin-1 and Murf-1) were evaluated in the late phase. In the early phase, left ventricular dimensions and wall stress were smaller in the SVR group than in the sham group, whereas they were comparable in the late period. Myocyte area in the SVR group was reduced to the value in the control group, while it was larger in the sham group than in the control group. Total-AMPKα, p-AMPKα, and AMPKα phosphorylation rates were higher, and Atrogin-1 and Murf-1 were lower in the SVR group than in the sham group, while the autophagy markers were not different between the groups. p-AMPKα had strong negative correlations with myocyte area, Atrogin-1, and Murf-1.
Conclusions:In myocyte reverse remodeling after SVR, AMPKα phosphorylation increased in association with reduced gene expression of ubiquitin ligases.
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