Breast reconstruction using a superficial inferior epigastric artery flap with pedicle elongation via an arteriovenous loop: A case report.

Superficial inferior epigastric artery (SIEA) flap is often chosen to minimize postoperative complications such as abdominal pain and bulging. However, drawbacks, including a small diameter and a short pedicle, pose challenges in anastomosing or creating the lower pole of the breast. Here, we report a case of breast reconstruction using an SIEA flap with pedicle elongation via an arteriovenous loop (AV-loop) using a contralateral superficial inferior epigastric vein (SIEV) graft. A 49-year-old woman underwent a left total mastectomy with the primary insertion of a tissue expander. Breast reconstruction using an SIEA flap with pedicle elongation was planned. The running pattern, pedicle length, and diameter of bilateral SIEA/SIEV and superficial circumflex iliac artery and vein (SCIA/SCIV) were evaluated preoperatively using a 48-MHz probe of ultra-high-frequency ultrasonography (Vevo MD ultrasound device, Fujifilm Visual Sonics, Amsterdam, the Netherlands). During the flap harvesting, the contralateral SIEV graft was harvested to create an AV-loop for pedicle elongation. The 9 cm graft was anastomosed to the left internal mammary artery and vein (IMA/IMV). After the flap elevation, the created AV-loop was divided at the midpoint and anastomosed to the pedicle of the SIEA flap. The SIEA flap, extended with a SIEV AV-loop, facilitated the augmentation of the lower pole of the breast without the risk of pedicle kinking and pulling. The postoperative course was uneventful, and the patient was discharged on postoperative day 7. The prolonged pedicle length via an AV-loop prevents the pedicle kinking and allows for positioning the flap more freely, resulting in an aesthetically good breast contour by filling in the lower pole. The precise preoperative evaluation of the vessels using ultra-high-frequency ultrasonography facilitated meticulous planning. In cases where surgeons aim to minimize intraoperative and postoperative complications associated with other abdominal free flaps, this method may be considered a viable and promising option.

Caveolae-specific activation loop between CaMKII and L-type Ca2+ channel aggravates cardiac hypertrophy in α1-adrenergic stimulation.

Activation of CaMKII induces a myriad of biological processes and plays dominant roles in cardiac hypertrophy. Caveolar microdomain contains many calcium/calmodulin-dependent kinase II (CaMKII) targets, including L-type Ca2+ channel (LTCC) complex, and serves as a signaling platform. The location of CaMKII activation is thought to be critical; however, the roles of CaMKII in caveolae are still elusive due to lack of methodology for the assessment of caveolae-specific activation. Our aim was to develop a novel tool for the specific analysis of CaMKII activation in caveolae and to determine the functional role of caveolar CaMKII in cardiac hypertrophy. To assess the caveolae-specific activation of CaMKII, we generated a fusion protein composed of phospholamban and caveolin-3 (cPLN-Cav3) and GFP fusion protein with caveolin-binding domain fused to CaMKII inhibitory peptide (CBD-GFP-AIP), which inhibits CaMKII activation specifically in caveolae. Caveolae-specific activation of CaMKII was detected using phosphospecific antibody for PLN (Thr17). Furthermore, adenoviral overexpression of LTCC ß2a-subunit (ß2a) in NRCMs showed its constitutive phosphorylation by CaMKII, which induces hypertrophy, and that both phosphorylation and hypertrophy are abolished by CBD-GFP-AIP expression, indicating that ß2a phosphorylation occurs specifically in caveolae. Finally, ß2a phosphorylation was observed after phenylephrine stimulation in ß2a-overexpressing mice, and attenuation of cardiac hypertrophy after chronic phenylephrine stimulation was observed in nonphosphorylated mutant of ß2a-overexpressing mice. We developed novel tools for the evaluation and inhibition of caveolae-specific activation of CaMKII. We demonstrated that phosphorylated ß2a dominantly localizes to caveolae and induces cardiac hypertrophy after α1-adrenergic stimulation in mice.NEW & NOTEWORTHY While signaling in caveolae is thought to be important in cardiac hypertrophy, direct evidence is missing due to lack of tools to assess caveolae-specific signaling. This is the first study to demonstrate caveolae-specific activation of CaMKII signaling in cardiac hypertrophy induced by α1-adrenergic stimulation using an originally developed tool.